Case of primary pulmonary cryptococcosis accompanied by severe back pain]

We report a case of primary pulmonary cryptococcosis. A 43-year-old male, without any significant underlying disease or immunological abnormalities, was admitted to our hospital with a complaint of sudden onset of severe back pain. His chest-X-ray and computed tomography revealed infiltrative shadows in the left lower lung without any signs of pleural effusion. Through transbronchial biopsy, cryptococcosis was obtained. Cryptococcal antigen also tested positive, we diagnosed this case as primary pulmonary cryptococcosis. And started anti-fungal therapy (fluconazole) consisting of parenteral and oral fluconazole. As soon as anti-fungal therapy was started, both the chest X-ray findings and cryptococcal antigen showed general improvement. Furthermore, subjective symptoms subsided immediately after treatment, During follow up through the outpatient clinic, his symptomatic complaint and chest roentgenogram shows improvements. This case was noteworthy for two reasons: 1) In cases with chest X-rays showing infiltrative shadows but lacking any underlying diseases, pulmonary cryptococcosis should be considered. 2) Sudden onset of back pain is a rare but a possible primary symptom of pulmonary cryptococcosis.     

Infective endocarditis caused by lactobacillus

Lactobacillus (LB) is a gram-positive rod-shaped bacterium that inhabits the oral cavity, gastrointestinal tract, vagina and nasal cavity. Although LB plays a role in the prevention of infections caused by pathogenic bacteria, it causes some critical infectious diseases such as infective endocarditis (IE). IE due to LB is rare; however, early diagnosis and early treatment are important because of its high mortality rate. We report the onset of IE after otologic treatment in a heavy drinker of alcohol, the second case of IE due to LB in Japan.     

Lnk prevents inflammatory CD8+ T‐cell proliferation and contributes to intestinal homeostasis

The intracellular adaptor Lnk (also known as SH2B3) regulates cytokine signals that control lymphohematopoiesis, and Lnk^?/? mice have expanded B‐cell, megakaryocyte, and hematopoietic stem‐cell populations. Moreover, mutations in the LNK gene are found in patients with myeloproliferative disease, whereas LNK polymorphisms have recently been associated with inflammatory and autoimmune diseases, including celiac disease. Here, we describe a previously unrecognized function of Lnk in the control of inflammatory CD8⁺ T‐cell proliferation and in intestinal homeostasis. Mature T cells from newly generated Lnk–Venus reporter mice had low but substantial expression of Lnk, whereas Lnk expression was downregulated during homeostatic T‐cell proliferation under lymphopenic conditions. The numbers of CD44^hiIFN‐γ⁺CD8⁺ effector or memory T cells were found to be increased in Lnk^?/? mice, which also exhibited shortening of villi in the small intestine. Lnk^?/? CD8⁺ T cells survived longer in response to stimulation with IL‐15 and proliferated even in nonlymphopenic hosts. Transfer of Lnk^?/? CD8⁺ T cells together with WT CD4⁺ T cells into Rag2‐deficient mice recapitulated a sign of villous abnormality. Our results reveal a link between Lnk and immune cell‐mediated intestinal tissue destruction.     

MICA/B expression in macrophage foam cells infiltrating atherosclerotic plaques

Infiltrating macrophages accumulate in fatty streak lesions and transform into foam cells, leading to the formation of atherosclerotic plaques. Inflammatory mechanisms underlying the plaque formation mediated by NKG2D-positive lymphocytes such as CD8⁺ T cells, natural killer cells and natural killer T cells have been extensively investigated. Yet, the involvement of the NKG2D system itself remains poorly understood. Recent work in mouse models has shown that blockade of an NKG2D receptor–ligand interaction reduces plaque formation and suppresses inflammation in aortae. In this study, we conducted immunohistochemical analysis of NKG2D ligand expression in autopsy-derived aortic specimens. Foam cells expressing NKG2D ligands MICA/B were found in advanced atherosclerotic lesions accompanied by a large necrotic core or hemorrhage. Human monocyte-derived macrophages treated in vitro with acetylated low-density lipoproteins enhanced expression of MICA/B and scavenger receptor A, thus accounting for NKG2D ligand expression in foam cells infiltrating atherosclerotic plaques. Our results suggest that, as in mice, the NKG2D system might be involved in the development of atherosclerosis in humans.     

Image-guided bronchoscopy for histopathologic diagnosis of pure ground glass opacity: a case report

Guided bronchoscopy has been found to be useful for the diagnosis of solid peripheral pulmonary lesions (PPLs) but more evidence on ground glass opacities (GGOs), especially those without a solid component, are lacking. A 69-year-old male, asymptomatic, heavy smoker was referred to our department for non-surgical diagnosis of a focal pure GGO in the right upper lobe that was found incidentally on computed tomography (CT). Transbronchial biopsy (TBB) with the aide of endobronchial ultrasound with a guide sheath (EBUS-GS), virtual bronchoscopic navigation (VBN), and fluoroscopy was performed for sampling. There were no complications after the procedure. The diagnosis of adenocarcinoma with lepidic growth pattern was established from the fourth and fifth TBB specimens and was confirmed on subsequent surgical resection. Image-guided bronchoscopy with TBB was successful for the diagnosis of a pure GGO. Use of a larger biopsy device may be helpful for the histopathologic diagnosis of lung adenocarcinoma with lepidic growth.     

Regulation of memory CD4 T-cell pool size and function by natural killer T cells in vivo

To develop more effective vaccines and strategies to regulate chronic inflammatory diseases, it is important to understand the mechanisms of immunological memory. Factors regulating memory CD4⁺ T helper (Th)-cell pool size and function remain unclear, however. We show that activation of type I invariant natural killer T (iNKT) cells with glycolipid ligands and activation of type II natural killer T (NKT) cells with the endogenous ligand sulfatide induced dramatic proliferation and expansion of memory, but not naïve, CD4 T cells. NKT cell-induced proliferation of memory Th1 and Th2 cells was dependent largely on the production of IL-2, with Th2-cell proliferation also affected by loss of IL-4. Type II NKT cells were also required for efficient maintenance of memory CD4 T cells in vivo. Activation of iNKT cells resulted in up-regulation of IFN-γ expression by memory Th2 cells. These IFN-γ–producing memory Th2 cells showed a decreased capability to induce Th2 cytokines and eosinophilic airway inflammation. Thus, activated NKT cells directly regulate memory CD4 T-cell pool size and function via the production of cytokines in vivo.