Klebsiella pneumoniae
successfully colonizes host tissues by recognizing and interacting with cholesterol present on membrane-associated lipid rafts. In this study, we evaluated the role of cholesterol in the expression of capsule polysaccharide genes of
K. pneumoniae
and its implication in resistance to phagocytosis. Our data revealed that exogenous cholesterol added to
K. pneumoniae
increases macrophage-mediated phagocytosis. To explain this event, the expression of capsular
galF, wzi
, and
manC
genes was determined in the presence of cholesterol. Down-regulation of these capsular genes occurred leading to increased susceptibility to phagocytosis by macrophages. In contrast, depletion of cholesterol from macrophage membranes led to enhanced expression of
galF, wzi
, and
manC
genes and to capsule production resulting in resistance to macrophage-mediated phagocytosis. Cholesterol-mediated repression of capsular genes was dependent on the RcsA and H-NS global regulators. Finally, cholesterol also down-regulated the expression of genes responsible for LPS core oligosaccharides production and OMPs. Our results suggest that cholesterol plays an important role for the host by reducing the anti-phagocytic properties of the
K. pneumoniae
capsule facilitating bacterial engulfment by macrophages during the bacteria-eukaryotic cell interaction mediated by lipid rafts.
Enterotoxigenic
Escherichia coli
produces a myriad of adhesive structures collectively named colonization factors (CFs). CS3 is a CF, which is assembled into fine wiry fibrillae encoded by the
cstA-H
gene cluster. In this work we evaluated the influence of environmental cues such as temperature, osmolarity, pH, and carbon source on the expression of CS3 genes. The transcription of
cstH
major pilin gene was stimulated by growth of the bacteria in colonization factor broth at 37°C; the presence of glycerol enhanced
cstH
transcription, while glucose at high concentration, high osmolarity, and the depletion of divalent cations such as calcium and magnesium repressed
cstH
expression. In addition, we studied the role of H-NS, CpxRA, and CRP global regulators in CS3 gene expression. H-NS and CpxRA acted as repressors and CRP as an activator of
cstH
expression. Under high osmolarity, H-NS, and CpxRA were required for
cstH
repression. CS3 was required for both, bacterial adherence to epithelial cells and biofilm formation. Our data strengthens the existence of a multi-factorial regulatory network that controls transcription of CS3 genes in which global regulators, under the influence of environmental signals, control the production of this important intestinal colonization factor.
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