Mast cell degranulation induced by type 1 fimbriated Escherichia coli in mice.

Abstract

The strategic location of mast cells at the host-environment interface and their ability to release potent mediators of inflammation have suggested that these cells may play a pivotal role in host defense against bacterial infection. The ability of the opportunistic pathogen, Escherichia coli, to induce degranulation of mast cells obtained from the mouse peritoneum was investigated. We determined that unlike a mutant derivative deficient in the FimH subunit of the fimbriae or nonfimbriated E. coli, type 1 fimbriated E. coli induced mast cell degranulation in vitro. The magnitude of mast cell degranulation was directly proportional to the number of adherent bacteria on the cell surface in the initial period of the interaction. Using a mouse model of bacterial peritonitis, we demonstrated mast cell degranulation and histamine release by type 1 fimbriated bacteria in vivo. Furthermore, beads coated with FimH but not with FimA, the major subunit of type 1 fimbriae, evoked mast cell release of histamine in vivo in amounts comparable to that elicited by type 1 fimbriated E. coli. These studies reveal that mast cells can be degranulated by interaction with type 1 fimbriated E. coli and that FimH, the mannose-binding component of the fimbriae, is a potent mast cell stimulant. (J. Clin. Invest. 1994.

Harboring of Particulate Allergens within Secretory Compartments by Mast Cells following IgE/FcεRI-Lipid Raft-Mediated Phagocytosis

“…Labeling of TNP-PSGs with Alexa Fluor 488 or Alexa Fluor 633 was performed using Alexa Fluor 488 or Alexa Fluor 633 carboxylic acid succinimidyl ester, respectively. The E. coli strain used for these studies was ORN103(pUT2002), a nonadherent, fimbriated K-12 laboratory strain (21). TNP-E. coli was generated as described for TNP-PSG.…”

“…Because Ags found on common particulate allergens have not been characterized and the specific IgE Abs to these Ags are not readily available, we initiated our studies by generating a particulate allergen through the covalent binding of TNP moieties to an inert laboratory E. coli strain, ORN103(pUT2002) (21). TNP is routinely used as an Ag for in vitro assays because of the commercial availability of specific IgE Abs.…”

“…TNP is routinely used as an Ag for in vitro assays because of the commercial availability of specific IgE Abs. E. coli strain ORN103(pUT2002) possesses only 50% of the genome typically found on a clinical strain of E. coli and is devoid of any adhesive capabilities (21). We selected this particulate allergen model for several reasons.…”

MHC class II-dependent activation of CD4+ T cell hybridomas by human mast cells through superantigen presentation

“…In contrast, the involvement of these cells in defense against microorganisms has been demonstrated only in the last few years [4]. MC constitute a unique link between innate and acquired immunity because they express, on one hand, receptors for complement products [5] and bacterial and parasitic components [6,7] and, on the other hand, they express MHC class I molecules and Ig receptors, including high-affinity IgE receptors and different subtypes of IgG receptors. It is well known that the engagement of high-affinity IgE receptors or of certain types of IgG receptors on MC induces a cascade of events leading to MC activation and, as a consequence, to partial or complete release of stored and/or neosynthesized mediators including mediators of inflammation (histamine, proteoglycans, lipids), cytokines [interleukin (IL)-1, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, tumor necrosis factor ␣ (TNF-␣), platelet-derived growth factor (PDGF), granulocyte-macrophage colony-stimulating factor (GM-CSF)] and chemokines [IL-8, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein-1␣ (MIP-1␣), MIP-1␤] [8].…”

Internalization of FimH+ Escherichia coli by the human mast cell line (HMC-1 5C6) involves protein kinase C

“…In the presence of serum opsonins, this interaction resulted in loss of bacterial viability [3] followed by processing of bacterial antigens and eventual presentation of specific bacterial antigens to T cells [4]. These mast cell responses together with their intrinsic capacity to release a range of proinflammatory mediators on contact with bacteria or bacterial products [5] indicated that these cells play a critical role in host defense against infectious agents. That mast cells were indeed pivotal in host defense was recently demonstrated in in vivo studies where mast cell-deficient mice but not their congenic mast cell-sufficient counterparts were found to be highly susceptible to lethal bacterial infections [6][7][8][9].…”