Bacterial Interactions with Mucosal Epithelial Cells

Orihuela, Carlos J.; Tuomanen, Elaine; Fogg, George; DiRita, Victor J.

doi:10.1016/b978-012491543-5/50044-9

Cited by 4 publications

(4 citation statements)

References 133 publications

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“…This is particularly true for the encapsulated extracellular respiratory tract pathogens such as S. pneumoniae (Orihuela et al 2005). Yende et al and our own studies have shown elevated levels of IL-6 and TNFα are risk factors for CAP as a result of enhanced bacterial ligand expression (Yende et al 2005; Hinojosa et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Cellular senescence increases expression of bacterial ligands in the lungs and is positively correlated with increased susceptibility to pneumococcal pneumonia

Shivshankar

Boyd²,

Saux³

et al. 2011

Aging Cell

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107

108

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SummaryCellular senescence is an age-associated phenomenon that promotes tumor invasiveness owing to the secretion of proinflammatory cytokines, proteases, and growth factors. Herein we demonstrate that cellular senescence also potentially increases susceptibility to bacterial pneumonia caused by Streptococcus pneumoniae (the pneumococcus), the leading cause of infectious death in the elderly. Aged mice had increased lung inflammation as determined by cytokine analysis and histopathology of lung sections. Immunoblotting for p16, pRb, and mH2A showed that elderly humans and aged mice had increased levels of these senescence markers in their lungs vs. young controls. Keratin 10 (K10), laminin receptor (LR), and platelet-activating factor receptor (PAFr), host proteins known to be co-opted for bacterial adhesion, were also increased. Aged mice were found to be highly susceptible to pneumococcal challenge in a PsrP, the pneumococcal adhesin that binds K10, dependent manner. In vitro senescent A549 lung epithelial cells had elevated K10 and LR protein levels and were up to 5-fold more permissive for bacterial adhesion. Additionally, exposure of normal cells to conditioned media from senescent cells doubled PAFr levels and pneumococcal adherence. Genotoxic stress induced by bleomycin and oxidative stress enhanced susceptibility of young mice to pneumonia and was positively correlated with enhanced p16, inflammation, and LR levels. These findings suggest that cellular senescence facilitates bacterial adhesion to cells in the lungs and provides an additional molecular mechanism for the increased incidence of communityacquired pneumonia in the elderly. This study is the first to suggest a second negative consequence for the senescence-associated secretory phenotype.

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Section: Discussionmentioning

confidence: 99%

Cellular senescence increases expression of bacterial ligands in the lungs and is positively correlated with increased susceptibility to pneumococcal pneumonia

Shivshankar

Boyd²,

Saux³

et al. 2011

Aging Cell

Self Cite

107

108

View full text Add to dashboard Cite

show abstract

“…The mucosal microbiota, epithelial cells, and the mucosal immune system constitute a stable and interdependent "tripod" that maintains mucosal homeostasis by complex mechanisms [3,4,6,[24][25][26][27][28]. For example, epithelial cells display surface receptors that are selectively exploited by bacteria adhering to their apical surfaces [1,2,[28][29][30], and express the basolateral membrane receptor (polymeric Ig receptor; pIgR) that transports locally produced polymeric (p) IgA into the external secretions [23]. Bacteria 0165-2478/$ -see front matter © 2009 Elsevier B.V. All rights reserved.…”

Section: Role Of Secretory Iga (S-iga) In Mucosal Immunitymentioning

confidence: 99%

Specific antibody activity, glycan heterogeneity and polyreactivity contribute to the protective activity of S-IgA at mucosal surfaces

Městecký

Russell

2009

Immunology Letters

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An explanation of the principles and mechanisms involved in peaceful co-existence between animals and the huge, diverse, and ever-changing microbiota that resides on their mucosal surfaces represents a challenging puzzle that is fundamental in everyday survival. In addition to mechanical barriers and a variety of innate defense factors, mucosal immunoglobulins (Igs) provide protection by two complementary mechanisms: specific antibody activity and innate, Ig glycan-mediated binding, both of which serve to contain the mucosal microbiota in its physiological niche. Thus, the interaction of bacterial ligands with IgA glycans constitutes a discrete mechanism that is independent of antibody specificity and operates primarily in the intestinal tract. This mucosal site is by far the most heavily colonized with an enormously diverse bacterial population, as well as the most abundant production site for antibodies, predominantly of the IgA isotype, in the entire immune system. In embodying both adaptive and innate immune mechanisms within a single molecule, S-IgA maintains comprehensive protection of mucosal surfaces with economy of structure and function.

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“…Paradoxically, attachment of many respiratory tract pathogens to epithelial cells is facilitated by the induction of a proinflammatory response, which causes the upregulation of surface proteins the bacteria co-opts for adhesion [106,107]. This is one reason elderly humans, who exhibit chronic low-grade inflammation, are at risk for more severe pneumonia caused by these commensal bacteria [108].…”

Section: Immune Quiescence Through Altered Virulence Determinant Prodmentioning

confidence: 99%

Future Perspective on Host–Pathogen Interactions During Bacterial Biofilm Formation within the Nasopharynx

Blanchette

Orihuela

2012

Future Microbiol.

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Nasopharyngeal colonization provides bacteria with a place of residence, a platform for person-to-person transmission and for many opportunistic pathogens it is a prerequisite event towards the development of invasive disease. Therefore, how host factors within the nasopharynx contribute to, inhibit or otherwise shape biofilm formation, the primary mode of existence for colonizing bacteria, and how biofilm bacteria subvert the acute inflammatory response that facilitates clearance, are important topics for future microbiological research. This review proposes the examination of host components as bridging molecules for bacterial interactions during biofilm formation, altered virulence determinant production and cell wall modification as a mechanism for immunoquiescence, and the role of host factors as signals and co-opted mechanisms for bacterial dissemination, together providing an opportunity for disease.

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Bacterial Interactions with Mucosal Epithelial Cells

Cited by 4 publications

References 133 publications

Cellular senescence increases expression of bacterial ligands in the lungs and is positively correlated with increased susceptibility to pneumococcal pneumonia

Cellular senescence increases expression of bacterial ligands in the lungs and is positively correlated with increased susceptibility to pneumococcal pneumonia

Specific antibody activity, glycan heterogeneity and polyreactivity contribute to the protective activity of S-IgA at mucosal surfaces

Future Perspective on Host–Pathogen Interactions During Bacterial Biofilm Formation within the Nasopharynx

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