B-1 lymphocytes are able to produce IL-10, but is not pathogenic during Leishmania (Leishmania) amazonensis infection |
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| Affiliation: | 1. Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil;2. Núcleo Multidisciplinar de Pesquisa UFRJ – Xerém em Biologia (NUMPEX-BIO), Campus Duque de Caxias Professor Geraldo Cidade – Universidade Federal do Rio de Janeiro, Duque de Caxias, Rio de Janeiro, Brazil;3. Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Brazil;4. Núcleo de Doenças Infecciosas/ Núcleo de Biotecnologia- Universidade Federal do Espírito Santo, Vitória, Espírito Santo, Brazil;5. Laboratório de Imunopatologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Brazil;6. Faculdade de Medicina, Centro de Pesquisa em Tuberculose, Universidade Federal do Rio de Janeiro, Brazil;7. Instituto de Veterinária, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ, Brazil;1. University of Chile, Faculty of Physical and Mathematical Sciences, CeBiB, Chile;2. University of Chile, Faculty of Medicine, ICBM, Immunology Disciplinary Program, Chile;3. University of Chile, Faculty of Medicine, Anatomy and Developmental Biology Disciplinary Program, ICBM, Experimental and Molecular Embryology Laboratory, Chile;1. Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450052, Henan, China;2. Academy of Medical Science, Zhengzhou University, Zhengzhou, 450001, Henan, China;3. Henan Key Laboratory of Tumor Epidemiology, Zhenghzou University, Zhengzhou, 450052, Henan, China;4. Department of Clinical Laboratory, Fuwai Central China Cardiovascular Hospital, Zhengzhou, 451464, Henan, China;5. Department of Clinical Laboratory, Zhengzhou Hospital of Traditional Chinese Medicine, Zhengzhou, 450000, Henan, China;1. Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, United States;2. Molecular and Cellular Biology Program, Ohio University, United States;3. Biomedical Engineering Program, Russ College of Engineering and Technology, Ohio University, United States;4. The Diabetes Institute at Ohio University, United States;1. Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA;2. Department of Diagnosis and Surgery, UNESP-State University of Sao Paulo, School of Dentistry at Araraquara, Araraquara, SP, Brazil;3. Department of Physical Therapy, University of Florida Health Science Center, Gainesville, FL, USA;4. Department of Stomatology, School of Dentistry, Federal University of Goias (UFG), Goiania, GO, Brazil;5. Department of Foundational Sciences, College of Dental Medicine, East Carolina University, Greenville, NC, USA;1. Singapore Immunology Network (SIgN), A*STAR, Singapore;2. Department of Microbiology and Immunology, National University of Singapore (NUS), Singapore, Singapore;1. Institute of Health Sciences, Department of Clinical Medicine, Laboratory of Experimental Immunopharmacology, Federal University of Triângulo Mineiro, Uberaba, MG, 38025-350, Brazil;2. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA;3. Laboratory of Immunology and Infectious Diseases, Triângulo Mineiro Federal University, Uberaba, Brazil |
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| Abstract: | Over the years research has found an association between B lymphocytes and pathogenesis during Leishmania sp. infections. Recently we demonstrated that B-2 lymphocytes are the main producers of IL-10 during L. amazonensis infection, and that the disease severity in BALB/c mice was attributed to these IL-10-producing B-2 lymphocytes. Here, we aim to understand the role of peritoneal B-1 lymphocytes in the pathogenesis of L. amazonensis infection. We found that infection resulted in a decrease in the number of B-1a lymphocytes and increase in B-1b lymphocytes in the peritoneal cavity of WT BALB/c mice but not in B lymphocyte deficient mice (BALB/Xid) mice. In vitro interaction between B-1 lymphocytes and L. amazonensis showed that the amastigote form of the parasite was able to induce higher levels of IL-10 in B-1 lymphocytes derived from infected BALB/c mice than the promastigote. Moreover, B-1 lymphocytes derived from infected mice produced more IL-10 than B-1 lymphocytes derived from naïve mice under amastigote interaction. However, the repopulation of BALB/Xid mice with B-1 lymphocytes from WT BALB/c mice did not affect the lesion development. Together, these results suggest that although B-1 lymphocytes are able to produce IL-10 during in vitro interaction with L. amazonensis, they are not directly related to pathogenesis in vivo. |
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| Keywords: | Leishmania amazonensis B-1 IL-10 XID BALB/c |
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