Mast cells and histamine alter intestinal permeability during malaria parasite infection

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• 作者：Rashaun A. Potts ^{rapotts@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Caitlin M. Tiffany ^{cmtiffany@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Nazzy Pakpour ^{npakpour@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Kristen L. Lokken ^{kllokken@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Connor R. Tiffany ^{crtiffany@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Kong Cheung ^{kcheung@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; René ; e M. Tsolis ^{rmtsolis@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author} ; Shirley Luckhart ; ^{sluckhart@ucdavis.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：NTS ; non-typhoidal Salmonella serotypes ; GI ; gastrointestinal ; RBC ; red blood cell ; H1 ; histamine receptor 1 ; H2 ; histamine receptor 2 ; i.p. ; intraperitoneally ; CFU ; colony forming units ; PBS ; phosphate-buffered saline ; LB ; Luria&ndash ; Bertani medium ; TBST ; Tris-buffered Saline ; IL ; interleukin (IL-10 ; 4 ; 6) ; TNF-α ; tumor necrosis factor alpha ; IFNγ ; interferon gamma ; B2  ; M ; beta-2-microglobulin ; EcN ; Escherichia coli Nissle ; NO ; nitric oxide
• 刊名：Immunobiology
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：221
• 期：3
• 页码：468-474
• 全文大小：1819 K

文摘

Co-infections with malaria and non-typhoidal Salmonella serotypes (NTS) can present as life-threatening bacteremia, in contrast to self-resolving NTS diarrhea in healthy individuals. In previous work with our mouse model of malaria/NTS co-infection, we showed increased gut mastocytosis and increased ileal and plasma histamine levels that were temporally associated with increased gut permeability and bacterial translocation. Here, we report that gut mastocytosis and elevated plasma histamine are also associated with malaria in an animal model of falciparum malaria, suggesting a broader host distribution of this biology. In support of mast cell function in this phenotype, malaria/NTS co-infection in mast cell-deficient mice was associated with a reduction in gut permeability and bacteremia. Further, antihistamine treatment reduced bacterial translocation and gut permeability in mice with malaria, suggesting a contribution of mast cell-derived histamine to GI pathology and enhanced risk of bacteremia during malaria/NTS co-infection.