Action of metabolic hormones on the fine structure of rat liver cells III. Effects of adrenalectomy and administration of cortisone

Electron microscopic studies were made of hepatocytes from sham-operated rats, adrenalectomized animals fasted 15 hours, and adrenalectomized rats fasted 15 hours but given a single I.P. injection (10 mg) of cortisone acetate. The objective of this work was to define the earliest morphological response of hepatocytes to injection of a glucocorticoid and to provide additional information on the mechanism of hormone action at the cellular level. Hepatocytes from fasted, adrenalectomized rats contained no glycogen particles and very little smooth endoplasmic reticulum (SER). In addition the rough endoplasmic reticulum was disorganized and showed fewer ribosomes and polysomes than found in liver cells from sham-operated rats. Two hours after glucocorticoid injection glycogen particles were seen in numerous centrilobular cells and some periportal hepatocytes. Elements of SER were associated with the glycogen particles. By 4 hours after hormone injection abundant glycogen was found in all hepatocytes. Centrilobular cells showed dispersed glycogen with extensive tubules of SER associated with the glycogen particles. Periportal hepatocytes accumulated glycogen as dense masses scattered throughout the cytosome. SER occurred mainly at the edges of the glycogen masses. Midlobular cells showed glycogen patterns intermediate between periportal and centrilobular cells; masses of dispersed glycogen with abundant SER occurred within and around the glycogen areas of the cells. Glucocorticoid stimulation also caused cisternae of RER to align in parallel arrays, and more ribosomes and polysomes appeared on membranes of RER than in similar cells from adrenalectomized rats. The interpretation is offered that the glucocorticoid-stimulated proliferation of SER is the morphological expression of induced microsomal enzyme synthesis (glucose-6-phosphatase) known to occur under these hormonal conditions.     

Relationships between IgG, IgM, IgE and resistance to reinfection during the early phase of infection with Clonorchis sinensis in rats

An enzyme linked immunosorbent assay (ELISA) was used to study the correlation between the levels of IgG, IgM and IgE immunoglobulin isotypes and resistance to reinfection in rats during the first month of infection with Clonorchis sinensis. Rats were infected with Clonorchis sinensis (primary infection), and then treated with praziquantel on the 1st, 3rd, 7th, 14th and 28th day post infection (p.i.). To measure resistance, rats were re-infected with C. sinensis (secondary infection), 2 weeks after the treatment and worms were recovered 4 weeks later. During the primary infection, significantly increased levels of IgG isotype were observed on days 14 and 28 p.i. (P < 0.001) and IgM levels were significantly increased on 3rd and 28th day (P < 0.001). During the secondary infection, significantly increased levels of IgG isotype were found from 3rd to 28th day and IgE isotype on 7th and 14th day (P < 0.01) while significant levels of IgM were found on the 3rd and 28th day (P < 0.05). Furthermore, significant differences of worm numbers between infected and control group was found on the 14th and 28th day (P < 0.001). An inverse correlation betwee the IgG levels and the resistance to re-infection was also observed (r = -0.948, P = 0.004), indicating that the resistance to reinfection is highly associated with the levels of IgG during the early phase of infection, and then with the IgM and IgE.     

Action of metabolic hormones on the fine structure of liver cells. II. Effects of hypophysectomy and chronic administration of somatotropin

Electron microscopic studies of hepatocytes from sham-operated, hypophysectomized, and hypophysectomized rats treated with somatotropin were undertaken in order to obtain morphological information on the mechanism of hormone action at the cellular level. Fed and fasted animals from each of the above groups were studied. Hepatocytes from fed rats of the three groups showed similar characteristics: periportal cells contained large dense masses of glycogen throughout the cytosome with relatively little smooth endoplasmic reticulum; mid-lobular cells displayed small dense masses of glycogen with few associated elements of smooth endoplasmic reticulum; centrilobular hepatocytes showed dispersed glycogen and abundant smooth endoplasmic reticulum. Hepatocytes from hypophysectomized rats fasted fifteen hours showed significant alterations in structure when compared with liver cells from sham-operated animals. Differences noted were: decrease in mid-lobular cell size and amount of smooth endoplasmic reticulum; decrease in glycogen, number of ribosomes and polysomes per hepatocyte; disorganization of the rough endoplasmic reticulum; and swelling of mitochondria and increase in number per cytoplsmic volume. Periportal hepatocytes from fasted hypophysectomized rats treated with somatotropin for ten days contain numerous small masses of glycogen with elements of smooth endoplasmic reticulum at the periphery of the glycogen masses. Mid-lobular and centrilobular hepatocytes contain masses of dispersed glycogen with an abundance of smooth endoplasmic reticulum associated with the glycogen particles.     

Effect of Toxoplasma gondii infection kinetics on trophoblast cell population in Calomys callosus,a model of congenital toxoplasmosis

This work evaluated the kinetics of events that occur in the placenta of Calomys callosus after Toxoplasma gondii infection. Animals on the first day of pregnancy (dop) and virgin nonpregnant females were perorally infected with 20 cysts of T. gondii strain ME49. After 100 days of infection, the virgin animals were mated and received an additional 20 cysts on the first dop. The placentas and the embryos from both acutely and chronically infected animals were analyzed up to day 20 of pregnancy by morphological and immunocytochemical assays. Noninfected and infected animals exhibited placenta with normal morphology. From the seventh dop and infection onwards, liver and spleen cells of the infected animals contained several parasitophorous vacuoles. On the 13th day, the maternal blood present at the placental blood spaces contained T. gondii-infected leukocytes. Infected placental cells were only seen on the 15th dop, being the trophoblast giant cells, the first cell type to contain signs of the parasite internalization, followed by labyrinth zone cells 24 h later and spongiotrophoblast cells only after the 19th dop. Fetal liver and brain were infected by T. gondii concomitantly to the labyrinth cell infection. No signals of infection were observed on placentas and embryos from chronically infected animals. Therefore, considering the sequence of events leading to the infection of the various organs, it could be hypothesized that the placenta is infected later on during pregnancy, which may be related to the defense roles played by this structure. However, trophoblast giant cells are unable to completely stop the progression of T. gondii infection towards the fetal tissues. C. callosus was demonstrated to be a suitable experimental model to study the dynamics of congenital toxoplasmosis.     

Echinostoma caproni in rats: worm population dynamics and host blood eosinophilia during primary infections with 6, 25 and 50 metacercariae and resistance to secondary and superimposed infections

Hooded-Lister rats were inoculated with 6, 25, 50 or 100 metacercariae of the intestinal trematodeEchinostoma caproni. Worm establishment and the pattern of egg excretion were followed during the course of primary infections with 6, 25 and 50 metacercariae. Peripheral blood eosinophilia was followed at all infecton levels. After 1 month, worm recovery and faecal egg output showed a gradual decline with increasing duration of infection. High worm burdens were expelled later than smaller worm burdens, and egg output persited longer in animals exhibiting a high initial egg out-put. The level of blood eosinophilia increased with increasing degree of infection and with the level of egg output. A marked concomitant resistance to superimposed infection was observed on the challenge of rats harbouring 21- and 49-day-old infections with 50 metacercariae. In addition, rats were partially resistant to secondary infection at challenge day 14 following anthelmintic removal of primary 7-day-old infections with 50 metacercariae and were completely resistant at challenge day 7 following elimination of a primary 14-day-old primary infection.     

Comparative study of Rosette- and plaque-formation in rats infected withMycoplasma arthritidis andAcholeplasma laidlawii

Mycoplasma arthritidis was shown to inhibit rosette and plaque formation in rats infected with this species of mycoplasma. By the 15th day the immune response in the control and experimental groups was equal again. At later stages strong stimulation of populations of rosette-forming (RFC) plaque-forming (PFC) cells was observed, subsiding toward the 150th day. Conversely,Acholeplasma laidlawii stimulates RFC and PFC at all periods of infection. The relatinship between these phenomena and the pathogenic properties of mycoplasmas is discussed.N. F. Gamaleya Institute of Epidemiology and Microbiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR O. V. Baroyan.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 7, pp. 68–71, July, 1979.     

不同剂量内毒素刺激枯否细胞分泌肿瘤坏死因子-α及内皮素-1的体外观察

目的：探讨体外脂多糖(LPS)刺激枯否细胞(KC)分泌肿瘤坏死因子-α(TNF-α)及内皮素-l(ET-1)的作用。方法：采用大鼠肝KC分离与培养技术,动态观察LPS刺激KC分泌TNF-α和ET-l的作用。结果：LPS具有明显活化KC作用,在一定浓浓度范围内对KC分泌的TNF-α及ET-l有促进作用。结论：LPS可促进体外培养的KC分泌TNF-α及ET-1,这可能与内毒素血症导致的肝损伤有关。     

Comparative histochemical studies of rats infected with a pathogenic and nonpathogenic trypanosome

Histochemical variations in tissues from rats inoculated with Trypanosoma lewisi and Trypanosoma rhodesiense were investigated. During peak parasitemia, the liver of rats inoculated with T lewisi showed increased glycogen distribution. However, glycogen depletion was noted in the liver and spleen of animals inoculated with living cells of T rhodesiense. Depletion was very apparent from day 4 to day 10. Throughout the period of observation, only a small amount of lipid infiltration occurred in tissues from animals inoculated with both organisms. Protein tests revealed a normal distribution of protein in tissues. Sections of the liver from rats inoculated with T lewisi showed strong alkaline phosphatase activity on days 7, 10, and 13. Alkaline phosphatase activity for T rhodesiense-infected animals was positive for days 4, 7, and 10. Strong positive reactions for acid phosphatase were observed on days 10 and 13 for some tissues (liver, spleen, and kidney) from rats inoculated with T lewisi. On days 4, 7, and 10, intense staining reactions also were observed for livers and spleens of animals inoculated with T rhodesiense. Regardless of tissues observed, histochemical variations were not observed in animals inoculated with the derivatives (ie, metabolic products and homogenates) of T lewisi and T rhodesiense.     

Relationship between neutrophil infiltration and tissue eosinophilia in the rat

Infection of rats with the parasite Mesocestoides corti increased the numbers of neutrophils, eosinophils and mononuclear cells in the blood. These peaked 11 days after infection and had declined to control levels by day 24. Increased number of eosinophils and mononuclear cells were also present in the peritoneal cavities of rats 24 days after infection. These gradually declined to reach control values by day 81. Intraperitoneal administration of glycogen to uninfected rats and to rats that had been infected for 24 and 81 days caused a transient increase in blood neutrophil numbers, maximal at 4 h. Although glycogen increased the numbers of neutrophils in the peritoneal cavities of uninfected animals and animals infected for 81 days, it did not increase the number of peritoneal neutrophils in rats that had been infected 24 days earlier. These results suggest that neutrophil infiltration can be impaired in animals undergoing an inflammatory response characterized by increased numbers of eosinophils.     

Metabolic adaptation to daily exercise of moderate intensity to exhaustion in the rat

Summary The rats were made to run daily to exhaustion, for 28 days at a speed of 1,200 m·h^–1 on a treadmill set at a gradient of + 10°. The training increased the time of running to exhaustion [184 (SD 49) and 308 (SD 28) min on the 1st and 28th day, respectively; P<0.001]. The body mass was reduced by training [257 (SD 21) g before and 221 (SD 20) g after; P<0.001] whereas the food intake increased [9 (SD 1) g·100 g^– body mass before and 14 (SD 2) g after; P0.001]. The heart mass was not affected by training. Training increased the resting glycogen concentration in muscles composed of different fibre types (soleus, white and red vastus muscles) and in the liver, but had no effect on its concentration in the heart and diaphragm. During exercise lasting for 30 min glycogen mobilization in the red vastus and soleus muscles and the liver was more pronounced after than before training. A sparing effect of training on the skeletal muscles and liver glycogen was markedly apparent only after exericse to exhaustion. The trained rats, contrary to the untrained, did not develop hypoglycaemia during exercise to exhaustion. An increase in the plasma free fatty acid concentration during exercise after training was delayed and attenuated compared to that before training. The 24-h excretion of urea after exercise to exhaustion on the 28th day of training was higher than on the 1st day by 39% (P<0.001). It is concluded that metabolic adaptation to training consisting of daily bouts of exercise to exhaustion differs in many aspects from that so far described for other endurance training protocols.     

Determination of serum and organ malondialdehyde (MDA) concentration, a lipid peroxidation index, in Trypanosoma brucei-infected rats

Lipid peroxidation was assessed in the sera and various organs of rats experimentally infected with Trypanosoma brucei. Thirty-six adult albino rats divided into 2 groups of eighteen rats each were used in this study. In experiment one, a group of 18 rats were used and they were divided into three groups (A, B and C) of six rats each. Groups B and C rats were infected with 1.54 × 10⁵ trypanosomes per rat intraperitoneally, whereas group A served as uninfected control. The rats were bled on day 0 and subsequently at 7-day intervals for packed cell volume (PCV), sera peroxidation index and parasitaemia. Also, temperature and weight were taken on day 0 and subsequently at 7-day intervals. In experiment 2, 18 rats were also used. Six rats each were sacrificed on days 0, 14 and 28-postinfection. Five rats each were sacrificed on day 14 and day 28 post-infection (PI) from group B, and their organs were promptly collected and washed with normal saline and used for organ malondialdehyde (MDA) concentration. The infection led to an increase in lipid peroxidation index (MDA concentration) of sera samples. The serum MDA concentration of the infected rat group was significantly (p < 0.01) higher than in the uninfected group on days 21 and 28 PI. The increase was however reversed by diminazene aceturate (Berenil; Hoechst, Ireland) treatment at the dosage of 7 mg/kg body weight administered on day 14 PI. The organ lipid peroxidation index also increased significantly (p < 0.05) in the eye, lung and spleen. However, there was no significant (p > 0.05) increase of lipid peroxidation index in the kidney, heart, liver, testes and brain. Also, the mean weekly MDA concentration increased as the disease progressed, the mean weekly temperature and parasitaemia also increased, but the reverse was the case with the mean weekly body weight and PCV which declined as the disease progressed. The findings are indication that oxidative stress plays an important role in the pathology of trypanosomosis.     

Trypanosoma lewisi: Cell populations and antibody formation in riboflavin deficient rats

Summary The influence of riboflavin deficiency on severity and duration of parasitemia was studied in Trypanosoma lewisi infected rats.The host dietary groups were: (1) complete or full complement; (2) riboflavin-deficient, and (3) pair-fed or calorically restricted. In all dietary groups, trypomastigotes appeared in peripheral tail blood of all inoculated rats after 7-day incubation periods. Riboflavin-deficient rats and pair-fed controls rats showed greater numbers of parasites than control-diet rats throughout the infection. The maximum parasitemia was on day 14 in control-diet rats; day 16 in riboflavin-deficient rats, and day 14 in pair-fed control rats. Parasitemia in riboflavin-deficient animals lasted 4 or more days longer than in the other two dietary groups.The average coefficients of variation in body length of trypomastigotes indicated that the formation of the reproduction inhibiting antibody (ablastin) was delayed seven days in riboflavin-deficient animals as compared with that in pair-fed and normal control animals.     

Circulating antigens and immune complexes in Schistosoma mansoni-infected rats. Characterization by radioimmunoprecipitation-PEG assay (RIPEGA)

Circulating schistosome antigens (CSA) and circulating immune complexes (CLC) were investigated in rats infected with Schistosoma mansoni. The radioimmunoprecipitation-polyethylene glycol (PEG) assay (RIPEGA), with 125I-labelled anti-S. mansoni anti-serum, detected CSA during two distinct periods of the infection; the first between the 11th and the 14th week of infection and the second between the 11th and 14th week after infection. The CH50 deviation test revealed the presence of CIC in sera from infected rats, approximately at the two periods when CSA were detected. At 6 weeks of infection, the levels of CIC in infected rats were not different from those in control rats. However, a more sensitive method characterized IgG2a in C1q-binding C1C from infected rats. At weeks 5 and 6, IgE immune complexes were also detected in the serum from infected rats. In fact, the use of RIPEGA on the material eluted from infected rat serum after passage through an anti-IgE immunosorbent showed the presence of schistosome antigen at week 4, and at higher levels at week 6. Levels of 50% haemolytic complement in infected rat serum were lowered between the 2nd and the 4th week, the 5th and the 8th week and after the 12th week of infection. The possible role played by CIC in the protective mechanisms to a S. mansoni challenge infection in rats is discussed.     

Flow microfluorometry analysis of alterations in T-lymphocyte subsets during murine listeriosis

C57BL/6 mice were infected intravenously with 6 X 10(3) Listeria monocytogenes organisms. As early as day 3 of infection, there was a marked reduction in the number of lymphocytes recovered from the peripheral blood, bone marrow, and thymuses of infected animals. Concomitantly, there was an increase in the number of splenic lymphocytes. By day 14, both the total and differential cell counts were similar in both infected and normal animals. Flow microfluorometric studies comparing the Thy-1.2, Lyt-1, Lyt-2, and surface immunoglobulin (SIg) phenotypes of lymphocytes from normal and infected mice were performed. Between days 3 and 5, there was a decrease in the percentage of Thy-1.2+ cells in the spleens of L. monocytogenes-infected animals. Conversely, the percentages of Lyt-1+, Lyt-2+, and SIg+ cells remained constant. At day 7 of infection, the percentage of Thy-1.2+ splenocytes was within normal limits, and at day 10, the percentage of Thy-1.2+ cells was elevated slightly. The absolute numbers of Thy-1.2+ cells were comparable in both infected and normal animals at early stages (days 3 to 5) of L. monocytogenes infection, but there was a marked elevation of Thy-1.2+ splenocytes at days 7 to 14 of infection. Lyt-1+, Lyt-2+, and SIg+ splenocytes increased in absolute numbers as early as day 3 of infection and were still elevated at day 14. Adrenalectomy before infection had no effect on the results obtained, suggesting that these changes were not mediated by endogenous steroids.     

小鼠肺泡发育与肺泡上皮细胞分化的电镜观察

目的　观察小鼠胚胎及生后肺泡发育及肺泡上皮分化。方法　小鼠胚胎 14天至生后 14天肺组织 ,隔天取材 ,HE染色光镜观察及透射电镜观察。结果　胚胎 14～ 18天 ,小鼠肺的发育以支气管树分支和管壁结构的逐渐完善为主 ,终蕾上皮为柱状或立方状的未分化细胞。胚胎 19天 ,支气管远端形成许多内壁光滑的原始肺泡 ,其上皮分化出Ⅱ型肺泡细胞。生后 1～ 4天 ,肺泡上皮出现少量扁平的Ⅰ型肺泡细胞 ,但仍以Ⅱ型肺泡细胞为主。生后 5～ 14天 ,成熟肺泡形成 ,肺泡上皮以Ⅰ型肺泡细胞为主。结论　出生时 ,小鼠的肺发育只完成了其大体形态的发生 ,肺泡上皮以Ⅱ型肺泡细胞为主。成熟肺泡的形成、数量的增加及Ⅰ型肺泡细胞的大量出现持续到出生后。     

Immune serum-mediated effects on brucellosis evolution in mice.

Immune serum injected into mice before a footpad challenge of virulent strain Brucella abortus 544 can prevent dissemination of infection to the spleen. Sera from mice infected with Brucella for at least 2 months or from mice vaccinated with a protein-bound cell wall peptidoglycan Brucella fraction completely stopped dissemination. Brucella lipopolysaccharide and polysaccharide cross-reacting Yersinia immune sera reduced dissemination. Both peptidoglycan and lipopolysaccharide immune sera injected simultaneously with an intravenous challenge caused a shift in Brucella from spleen to liver. When immune sera were injected simultaneously with an intravenous challenge, the kinetics of splenic infection showed two effects: an early one, optimally measured at day 7 postchallenge, showed reduced numbers in the spleen due to the shift of Brucella to the liver; a late effect, measured at day 21 postchallenge, showed reduced numbers in spleen and liver with nearly complete clearance by day 49 postchallenge. Brucella lipopolysaccharide and cross-reacting bacterial antisera induced the early effect only, whereas peptidoglycan and infected mouse sera induced both effects. When peptidoglycan immune serum was injected 2 or 7 days after intravenous challenge, the late effect was somewhat reduced. Hence, immune sera to protein and polysaccharide surface antigens can (i) prevent dissemination of systemic infection and (ii) help destroy intercellular bacteria (protein antigen only). These effects may represent a large part of vaccinal immunity.     

The role of the liver in immunity to blood-stage murine malaria.

Mice vaccinated with fixed parasitized red blood cells and Bordetella pertussis can clear an otherwise lethal Plasmodium yoelii infection in 7 days; this protection is abolished by splenectomy before vaccination. Most mice splenectomized following vaccination were able to clear their infections, although their recovery was delayed. When labelled parasitized red cells were injected into mice during an infection, splenic uptake fell from day 3 onwards while uptake by the liver increased. Lymphocytes (mainly T cells) formed the majority of the live cells extracted from livers 7 days after infection, although blasts and myeloid cells were also present. Infected livers from vaccinated mice contained most cells. Less marked increases were observed 7 days after P. berghei infection of vaccinated mice. Examination of liver tissue showed that the sinusoids contained increased numbers of cells and suggested that activation of Kupffer cells was occurring, particularly in vaccinated mice infected with P. yoelii. Homing experiments confirmed the increased trapping of various cells in livers of vaccinated mice infected with P. yoelii. These results suggest an important role for the liver in recovery from blood-stage malaria infection.     

Failure to demonstrate early metabolic changes in weanling growth-retarded hypophagic rats with lesions in the dorsomedial hypothalamic nuclei

Experiment 1: Weanling male rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated animals served as controls. Rats were killed four hours and three and seven days postoperatively (post-op). Plasma was obtained and epididymal fat pads, diaphragm and liver aliquots were harvested and the in vitro incorporation of U-14C-glucose into CO2, glycogen, lipid and saponifiable fatty acids (FAs) were measured. Body weight, carcass lipid and food intake were significantly lower in DMNL rats than in controls. The only significant lesion-induced metabolic changes were hypoglycemia and greater tracer incorporation into epididymal fat pad lipid and diaphragm glycogen. Both DMNL rats and controls showed similar time courses of tracer incorporation into epididymal CO2 and FAs, diaphragm lipid and liver CO2, glycogen, lipid and FAs. Lesioned rats also showed more pronounced decreases of tracer incorporation from day 0 to day 3 in epididymal glycogen and lipid and diaphragm CO2 and glycogen. These data make it appear unlikely that very early deficits in glucose metabolism are the cause of the growth retardation seen in long-term studies with DMNL rats. The data also demonstrate considerable locus specificity, since weanling rats with ventromedial hypothalamic lesions (VMNL rats) in similar short-term studies have shown dramatic alterations in the above parameters. Experiment 2: Weanling DMNL rats and sham-operated rats were injected via tail vein with tritiated water one hour post-op. One hour after the injection they were decapitated. There were no significant differences between DMNL rats and controls in mumoles tritiated water incorporated into total liver, grams liver tissue, mg liver glycogen and ml or mg plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of thyroid extract and triiodothyronine,with or without the addition of theophylline,on regeneration of the liver in rats

Starting from the day after operation, partly hepatectomized rats receivined thyroid or triiodothyronine separately or in conjunction with theophylline, by mouth. Thyroid and the thyroid hormone increased the oxygen consumption but considerably reduced the glycogen content of the liver. No statistically significant increase in the degree of regeneration hypertrophy, studied on the 7th day after the operation, was produced by these preparations. In conjunction with theophylline they increased the absolute and relative weight of the regenerating liver. The absolute weight of the liver was increased by 19–36%. The DNA content, the number of nuclei, and the number of binuclear cells were indistinguishable from the control.     

Intermittent Fasting Promotes Bacterial Clearance and Intestinal IgA Production in Salmonella typhimurium‐Infected Mice

The impact of intermittent fasting versus ad libitum feeding during Salmonella typhimurium infection was evaluated in terms of duodenum IgA levels, bacterial clearance and intestinal and extra‐intestinal infection susceptibility. Mice that were intermittently fasted for 12   weeks or fed ad libitum were infected with S. typhimurium and assessed at 7 and 14 days post‐infection. Next, we evaluated bacterial load in the faeces, Peyer's patches, spleen and liver by plate counting, as well as total and specific intestinal IgA and plasmatic corticosterone levels (by immunoenzymatic assay) and lamina propria IgA levels in plasma cells (by cytofluorometry). Polymeric immunoglobulin receptor, α‐ and J‐chains, Pax‐5 factor, pro‐inflammatory cytokine (tumour necrosis factor‐α and interferon‐γ) and anti‐inflammatory cytokine (transforming growth factor‐β) mRNA levels were assessed in mucosal and liver samples (by real‐time PCR). Compared with the infected ad libitum mice, the intermittently fasted infected animals had (1) lower intestinal and systemic bacterial loads; (2) higher SIgA and IgA plasma cell levels; (3) higher mRNA expression of most intestinal parameters; and (4) increased or decreased corticosterone levels on day 7 and 14 post‐infection, respectively. No contribution of liver IgA was observed at the intestinal level. Apparently, the changes following metabolic stress induced by intermittent fasting during food deprivation days increased the resistance to S. typhimurium infection by triggering intestinal IgA production and presumably, pathogen elimination by phagocytic inflammatory cells.