期刊
SCIENCE ADVANCES
卷 7, 期 27, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abd6232
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资金
- NIH/National Institute of Allergy and Infectious Disease grants [R01AI098078, R01AI112949, R21AI126860]
- Animal Models of Infectious Diseases Training Program NIH/NIAID [T32AI060555]
- China Scholarship Council
- NIH [T35OD010956]
- Postdoctoral Scholars Program at St. George's University
Infection with Plasmodium parasite weakens the host's resistance against Salmonella, leading to an increased colonization of Salmonella in the upper gastrointestinal tract. This may be due to the parasite-induced hypochlorhydria, which allows for enhanced survival of Salmonella in the stomach.
Malaria parasite infection weakens colonization resistance against Salmonella enterica serovar (S.) Typhimurium. S. Typhimurium is a member of the Enterobacterales, a taxon that increases in abundance when the colonic microbiota is disrupted or when the colonic mucosa is inflamed. However, here, we show that infection of mice with Plasmodium yoelii enhances S. Typhimurium colonization by weakening host control in the upper GI tract. P. yoeliiinfected mice had elevated gastric pH. Stimulation of gastric acid secretion during P. yoelii infection restored stomach acidity and colonization resistance, demonstrating that parasite-induced hypochlorhydria increases gastric survival of S. Typhimurium. Furthermore, blockade of P. yoelii-induced TNF-alpha signaling was sufficient to prevent elevation of gastric pH and enhance S. Typhimurium colonization during concurrent infection. Collectively, these data suggest that abundance in the fecal microbiota of facultative anaerobes, such as S. Typhimurium, can be increased by suppressing antibacterial defenses in the upper GI tract, such as gastric acid.
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