Host and microbiota factors that control Klebsiella pneumoniae mucosal colonization in mice

Lau, Helen Y.; Huffnagle, Gary B.; Moore, Thomas A.

doi:10.1016/j.micinf.2008.07.040

Cited by 46 publications

(37 citation statements)

References 31 publications

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“…Treatment of rats with indomethacin also changes their microbiome [82], implicating a relationship between mucosal inflammation and microbiome community structure. This concept is supported by other studies of gastrointestinal inflammation in which mucosal inflammation and epithelium damage drive changes in the indigenous microbiota, resulting in the outgrowth of γ-proteobacteria, such as E. coli and Klebsiella pneumoniae [83,84]. In a model of transmissible spontaneous colitis in mice, the transmissible bacterial community required the presence of K. pneumoniae and P. mirabilis in that community for mucosal inflammation [85].…”

Section: Could Changes In the Gastrointestinal Microbiome Affect Locamentioning

confidence: 56%

The microbiome in wound repair and tissue fibrosis

Scales

Huffnagle

2012

The Journal of Pathology

140

120

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Bacterial colonization occurs in all wounds, chronic or acute and the break in epithelium integrity that defines a wound impairs the forces that shape and constrain the microbiome at that site. This review highlights the interactions between bacterial communities in the wound and the ultimate resolution of the wound or development of fibrotic lesions. Chronic wounds support complex microbial communities comprised of a wide variety of bacterial phyla, genera and species, including some fastidious anaerobic bacteria not identified using culture-based methods. Thus, the complexity of bacterial communities in wounds has historically been underestimated. There are a number of intriguing possibilities to explain these results that may also provide novel insights into changes and adaptation of bacterial metabolic networks in inflamed and wounded mucosa, including the critical role of biofilm formation. It is well accepted that the heightened state of activation of host cells in a wound that is driven by the microbiota can certainly lead to detrimental effects on wound regeneration, but the microbiota of the wound may also have beneficial effects on wound healing. Studies in experimental systems have clearly demonstrated a beneficial effect for members of the gut microbiota on regulation of systemic inflammation, which could also impact wound healing at sites outside the gastrointestinal tract. The utilization of culture-independent microbiology to characterize the microbiome of wounds and surrounding mucosa has raised many intriguing questions regarding previously held notions about the cause and effect relationships between bacterial colonization and wound repair and mechanisms involved in this symbiotic relationship.

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Section: Could Changes In the Gastrointestinal Microbiome Affect Locamentioning

confidence: 56%

The microbiome in wound repair and tissue fibrosis

Scales

Huffnagle

2012

The Journal of Pathology

140

120

View full text Add to dashboard Cite

show abstract

“…One previous study determined that nasal colonization levels of Klebsiella pneumoniae were similar in GF and the corresponding WT mice (27), suggesting that the general immune deficiencies associated with these mice do not universally impact clearance mechanisms of the nasopharyngeal mucosa. In our system, where initial colonization is not limited by adaptive immunity in GF mice, it is possible that the normal murine flora promotes expression of cross-reactive antibodies recognizing broadly reactive targets that limit H. influenzae colonization.…”

Section: Discussionmentioning

confidence: 96%

Natural Antibody to Conserved Targets ofHaemophilus influenzaeLimits Colonization of the Murine Nasopharynx

Zola¹,

Лысенко²,

Weiser

2009

Infect Immun

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Nasopharyngeal colonization represents the initial interaction between Haemophilus influenzae and its human host. Factors that influence bacterial carriage likely affect transmission and incidence of infection. Therefore, we investigated host factors involved in limiting H. influenzae colonization in BALB/c mice, as colonization can be established in this genetic background. Unlike what is observed in the C57BL/6 background, initial colonization of BALB/c mice was mainly limited by adaptive immune components. This effect on colonization did not require either CD4-or CD8-positive T cells. Instead, initial colonization by genetically diverse strains was limited by preexisting natural antibody with a lesser contribution of complement activity and the presence of neutrophils. Natural serum immunoglobulin from mice was able to bind to the bacterial surface and exhibited complement-dependent bactericidal activity against these genetically diverse H. influenzae strains. Moreover, natural immunoglobulin G (IgG) recognizing these strains was detected at the nasopharyngeal mucosal surface. This antibody-mediated effect required exposure to the normal mouse microbial flora, since mice raised under germfree (GF) conditions showed increased levels of H. influenzae colonization that were not limited by adaptive immunity. In addition, serum IgG from GF mice exhibited less surface binding to H. influenzae, suggesting that natural antibody, induced through prior exposure to the microbial flora, mediated the observed reduction in initial colonization. The broad effect of natural IgG against genetically diverse isolates suggests the presence of conserved species-wide protective targets of antibody.

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“…K. pneumoniae and P. mirabilis can colonize the intestines of mice and humans (Lau et al, 2008). Notably, we only recovered these microbes from TRUC mice in our colony but not in Rag2 −/− or WT animals.…”

Section: Discussionmentioning

confidence: 99%

Enterobacteriaceae Act in Concert with the Gut Microbiota to Induce Spontaneous and Maternally Transmitted Colitis

Garrett

Gallini

Yatsunenko

et al. 2010

Cell Host & Microbe

705

599

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SUMMARY In inflammatory bowel disease, the relationship between a host and gut microbial community goes awry. We have characterized the fecal microbial communities in a mouse IBD model driven by T-bet deficiency in the innate immune system. 16S rRNA-based analysis of T-bet−/− × Rag2−/− and Rag2−/− mice revealed distinctive communities that correlate with host genotype. Culture-based surveys, invasion assays, antibiotic treatment, and TNF-α blockade disclosed that the presence of Klebsiella pneumoniae and Proteus mirabilis correlates with colitis in T-bet−/− × Rag2−/− animals, and that T-bet−/− × Rag2−/− derived strains can elicit colitis in Rag2−/− and wild-type adults. Cross-fostering experiments provided evidence for the role of these organisms in maternal transmission of disease. This model provides a foundation for defining how gut microbial communities work in concert with specific culturable colitogenic agents to cause IBD, and a foundation for conducting proof-of-concept tests of new preventative or therapeutic measures directed at components of the gut microbiota and/or host.

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Host and microbiota factors that control Klebsiella pneumoniae mucosal colonization in mice

Cited by 46 publications

References 31 publications

The microbiome in wound repair and tissue fibrosis

The microbiome in wound repair and tissue fibrosis

Natural Antibody to Conserved Targets ofHaemophilus influenzaeLimits Colonization of the Murine Nasopharynx

Enterobacteriaceae Act in Concert with the Gut Microbiota to Induce Spontaneous and Maternally Transmitted Colitis

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