Lymphoid tissue-resident Alcaligenes LPS induces IgA production without excessive inflammatory responses via weak TLR4 agonist activity

Shibata, Nao; Kunisawa, Jun; Hosomi, Koji; Fujimoto, Yukari; Mizote, Keisuke; Kitayama, Naohiro; Shimoyama, Atsushi; Mimuro, Hitomi; Sato, Shintaro; Kishishita, Natsuko; Ishii, Ken J.; Fukase, Koichi; Kiyono, Hiroshi

doi:10.1038/mi.2017.103

Cited by 56 publications

(73 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…46 Compared with E. coli LPS, LPS isolated from Alcaligenes only weakly activated dendritic cells to produce less IL-6, suggesting that the intensity of TLR4 signaling differs between bacterial LPS types. 47 Therefore, microfloral diversity or uniqueness may influence the signaling intensity of the intestinal TLR4-MyD88 pathway, which also is regulated by the LTB 4 -BLT1-MyD88 axis, for the production of antigen-specific IgA during oral vaccination.…”

Section: Discussionmentioning

confidence: 99%

BLT1 mediates commensal bacteria-dependent innate immune signals to enhance antigen-specific intestinal IgA responses

et al. 2019

Self Cite

View full text Add to dashboard Cite

Leukotriene B 4 receptor 1 (BLT1) triggers the migration of granulocytes and activated T cells; however, its role in B-cell function remains unclear. Here we report that BLT1 is required to induce the production of antigen-specific IgA against oral vaccine through mediating innate immune signals from commensal bacteria. B cells acquire BLT1 expression during their differentiation to IgA + B cells and plasma cells in Peyer's patches and the small intestinal lamina propria, respectively. BLT1 KO mice exhibited impaired production of antigen-specific fecal IgA to oral vaccine despite normal IgG responses to systemically immunized antigen. Expression of MyD88 was decreased in BLT1 KO gut B cells and consequently led to diminished proliferation of commensal bacteria-dependent plasma cells. These results indicate that BLT1 enhances the proliferation of commensal bacteria-dependent IgA + plasma cells through the induction of MyD88 and thereby plays a key role in the production of antigen-specific intestinal IgA.

show abstract

Section: Discussionmentioning

confidence: 99%

BLT1 mediates commensal bacteria-dependent innate immune signals to enhance antigen-specific intestinal IgA responses

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…18 Other commensals, such as Alcaligenes, naturally inhabit DCs within host PPs where they induce broadly mucosal IgA in a noninflammatory context. 25,26 These unique bacteria have likely co-evolved for millennia with the host because their levels drop in an IgA-deficient host, suggesting that IgA binding may be needed for their uptake and growth within gut-associated lymphoid tissue. 25 Additional commensals within lymphoid tissues promote tolerance by inducing interleukin (IL)-10 and IL-22 by DCs and innate lymphoid cells type 3, respectively, which collectively inhibit Th17 responses and facilitate bacterial colonization.…”

Section: Mechanisms Of Microbial Translocationmentioning

confidence: 99%

Mechanisms and consequences of gut commensal translocation in chronic diseases

et al. 2019

View full text Add to dashboard Cite

Humans and other mammalian hosts have evolved mechanisms to control the bacteria colonizing their mucosal barriers to prevent invasion. While the breach of barriers by bacteria typically leads to overt infection, increasing evidence supports a role for translocation of commensal bacteria across an impaired gut barrier to extraintestinal sites in the pathogenesis of autoimmune and other chronic, non-infectious diseases. Whether gut commensal translocation is a cause or consequence of the disease is incompletely defined. Here we discuss factors that lead to translocation of live bacteria across the gut barrier. We expand upon our recently published demonstration that translocation of the gut pathobiont Enterococcus gallinarum can induce autoimmunity in susceptible hosts and postulate on the role of Enterococcus species as instigators of chronic, noninfectious diseases.

show abstract

“…Within the PPs of mice, Alcaligenes spp., including A. faecalis, are a dominant genus among LRCs (Obata et al, 2010). Furthermore, after being taken up by M cells, A. faecalis is captured by CD11c + DCs in PPs (Sato et al, 2013;Shibata et al, 2018). Indeed, depletion of CD11c + DCs leads to the absence of A. faecalis in the PPs of mice (Shibata et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Lymphoid Tissue–Resident Alcaligenes Establish an Intracellular Symbiotic Environment by Creating a Unique Energy Shift in Dendritic Cells

Hosomi

Shibata²,

Shimoyama

et al. 2020

Front. Microbiol.

Self Cite

View full text Add to dashboard Cite

Lymphoid-tissue-resident commensal bacteria (LRCs), including Alcaligenes faecalis, are present in intestinal lymphoid tissue including the Peyer's patches (PPs) of mammals and modulate the host immune system. Although LRCs can colonize within dendritic cells (DCs), the mechanisms through which LRCs persist in DCs and the symbiotic relationships between LRCs and DCs remain to be investigated. Here, we show an intracellular symbiotic system in which the LRC Alcaligenes creates a unique energy shift in DCs. Whereas DCs showed low mitochondrial respiration when they were co-cultured with Escherichia coli, DCs carrying A. faecalis maintained increased mitochondrial respiration. Furthermore, E. coli induced apoptosis of DCs but A. faecalis did not. Regarding an underlying mechanism, A. faecalis-unlike E. coli-did not induce intracellular nitric oxide (NO) production in DCs due to the low activity of its lipopolysaccharide (LPS). Therefore, A. faecalis, an example of LRCs, may persist within intestinal lymphoid tissue because they elicit little NO production in DCs. In addition, the symbiotic DCs exhibit characteristic physiologic changes, including a low rate of apoptosis and increased mitochondrial respiration.

show abstract

Lymphoid tissue-resident Alcaligenes LPS induces IgA production without excessive inflammatory responses via weak TLR4 agonist activity

Cited by 56 publications

References 36 publications

BLT1 mediates commensal bacteria-dependent innate immune signals to enhance antigen-specific intestinal IgA responses

BLT1 mediates commensal bacteria-dependent innate immune signals to enhance antigen-specific intestinal IgA responses

Mechanisms and consequences of gut commensal translocation in chronic diseases

Lymphoid Tissue–Resident Alcaligenes Establish an Intracellular Symbiotic Environment by Creating a Unique Energy Shift in Dendritic Cells

Contact Info

Product

Resources

About