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1.
Environ Microbiol Rep ; 13(2): 138-158, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33314653

RESUMO

Coxiellosis or Q fever is an important global occupational zoonotic disease caused by one of the most contagious bacterial pathogens - Coxiella burnetii, which ranks one among the 13 global priority zoonoses. The detection of C. burnetii infection is exhibiting an increasing trend in high-risk personnel around the globe. It has increasingly been detected from foods of animal origin (including bulk milk, eggs, and meat) as well as tick vectors in many parts of the world. Coxiellosis is reported to be an important public health threat causing spontaneous abortions in humans and potential reproductive failure, which would result in production losses among livestock. Further, comprehensive coverage of the reports and trends of Q fever in developing countries, where this infection is supposed to be widely prevalent appears scarce. Also, the pathogen remains grossly neglected and underreported. Moreover, policymakers and funding agencies do not view it as a priority problem, especially in the Indian subcontinent, including Sri Lanka, Bhutan, Pakistan, Nepal, Bangladesh and Maldives. Here, we review the occurrence and epidemiology of the disease in a global context with special emphasis on its status in the Indian subcontinent.


Assuntos
Coxiella burnetii , Febre Q , Animais , Febre Q/epidemiologia , Zoonoses/epidemiologia
2.
Microorganisms ; 7(3)2019 Mar 02.
Artigo em Inglês | MEDLINE | ID: mdl-30832381

RESUMO

Type 1-diabetes (T1D) is an autoimmune disease characterized by immune-mediated destruction of pancreatic beta (ß)-cells. Genetic and environmental interactions play an important role in immune system malfunction by priming an aggressive adaptive immune response against ß-cells. The microbes inhabiting the human intestine closely interact with the enteric mucosal immune system. Gut microbiota colonization and immune system maturation occur in parallel during early years of life; hence, perturbations in the gut microbiota can impair the functions of immune cells and vice-versa. Abnormal gut microbiota perturbations (dysbiosis) are often detected in T1D subjects, particularly those diagnosed as multiple-autoantibody-positive as a result of an aggressive and adverse immunoresponse. The pathogenesis of T1D involves activation of self-reactive T-cells, resulting in the destruction of ß-cells by CD8⁺ T-lymphocytes. It is also becoming clear that gut microbes interact closely with T-cells. The amelioration of gut dysbiosis using specific probiotics and prebiotics has been found to be associated with decline in the autoimmune response (with diminished inflammation) and gut integrity (through increased expression of tight-junction proteins in the intestinal epithelium). This review discusses the potential interactions between gut microbiota and immune mechanisms that are involved in the progression of T1D and contemplates the potential effects and prospects of gut microbiota modulators, including probiotic and prebiotic interventions, in the amelioration of T1D pathology, in both human and animal models.

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