Innate Humoral Defense Factors

Russell, Michael W.; Bobek, Libuse A.; Brock, Jeremy H.; Hajishengallis, George; Tenovuo, Jorma

doi:10.1016/b978-012491543-5/50009-7

Cited by 14 publications

(10 citation statements)

References 222 publications

(141 reference statements)

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“…Found in mucosal exocrine secretions and in the secondary granules of neutrophils [2], Lf is considered an essential component of the host innate immune response [3]. It displays antibacterial activities associated with the inhibition of bacterial multiplication, probably by sequestering iron that is essential for bacterial growth [4] or by destabilizing the surface membrane of Gram negative bacteria after binding to outer membrane proteins [5] and LPS components such as Lipid A [6].…”

Section: Introductionmentioning

confidence: 99%

Lactoferrin increases both resistance to Salmonella typhimurium infection and the production of antibodies in mice

et al. 2010

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Section: Introductionmentioning

confidence: 99%

Lactoferrin increases both resistance to Salmonella typhimurium infection and the production of antibodies in mice

et al. 2010

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“…These virulence factors enable pneumococci to cause invasive disease, which results in more human deaths in developed countries than result from any other bacterial pathogen (12). However, since the reservoir of pneumococci is maintained primarily by human nasopharyngeal colonization, virulence factors that interfere with complement and phagocytosis make little sense at the mucosal surface, where there is little complement (28) and there are few phagocytes. One possible explanation for why pneumococci contain these disease-permitting virulence factors is that longterm nasal colonization involves more than simple surface adherence and actually requires invasion of mucosal tissue, where the pathogen has to defend itself against complement-dependent opsonization and phagocytosis.…”

mentioning

confidence: 99%

Nasal Colonization with Streptococcus pneumoniae Includes Subpopulations of Surface and Invasive Pneumococci

Briles

Novak

Hotomi³

et al. 2005

Infect Immun

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We demonstrated that during colonization with Streptococcus pneumoniae the nasal mucosal tissues of mice support two populations of pneumococci. Transparent-phase pneumococci can be readily washed from the outer surface, while a second population composed of primarily opaque-phase pneumococci is released only by homogenization of the nasal tissue. The fact that the opaque phase has previously been associated with invasion and the fact that opaque-phase pneumococci were released by homogenization of previously washed nasal tissue suggest that the opaque-phase pneumococci may have invaded the nasal tissue. Consistent with this hypothesis was our observation that there was inflammation in portions of the nasal mucosa of the colonized mice but not in the mucosa of noncolonized mice, but this observation did not prove the hypothesis. If the opaque-phase pneumococci released from the nasal tissue were from within the tissue and/or if resistance of the opaque-phase subpopulation to antibody, complement, and phagocytes is essential for long-term carriage, it seems likely that the virulence factors of S. pneumoniae that are necessary for killing humans exist to facilitate carriage. Although this speculation is unproven, the observation that there are separate populations of pneumococci during colonization may help guide future attempts to understand the biology of nasal colonization by this pathogen.Humans acquire Streptococcus pneumoniae invariably by asymptomatic nasal colonization (15). Transmission to others is thought to be primarily from colonized individuals. Even so, pneumococci possess virulence factors, including capsule, PspA, PspC, and pneumolysin, that allow them to resist the opsonic effects of complement deposition and thereby to avoid phagocytosis (1,10,22,26). These virulence factors enable pneumococci to cause invasive disease, which results in more human deaths in developed countries than result from any other bacterial pathogen (12). However, since the reservoir of pneumococci is maintained primarily by human nasopharyngeal colonization, virulence factors that interfere with complement and phagocytosis make little sense at the mucosal surface, where there is little complement (28) and there are few phagocytes. One possible explanation for why pneumococci contain these disease-permitting virulence factors is that longterm nasal colonization involves more than simple surface adherence and actually requires invasion of mucosal tissue, where the pathogen has to defend itself against complement-dependent opsonization and phagocytosis.Pneumococci have a phase shift that allows them to exist in transparent and opaque phases (36). Transparent-phase pneumococci have been shown to be released from nasal cavities of mice and infant rats by gentle washing with physiological salt solutions (36). In contrast, the majority of pneumococci recovered from the blood or lung are opaque-phase organisms (6,19,34). Moreover, it has been shown that nasal colonization in rodents is established more readily by transparent-phas...

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“…BPI is able to insert into the bacterial cell wall due to its hydrophobic core, increasing the cell wall permeability and leading to hydrolysis by the bacterial cell wall enzymes [51]. LTF is a non-heme iron binding protein and an essential component of the innate immune system [52]. It executes various protective functions for the host destabilizing bacterial membrane, inhibiting bacterial multiplication by altering membrane structure, enhancing the immunostimulatory effects, and binding with bacterial lipid A molecules [53].…”

Section: Discussionmentioning

confidence: 99%

Impact of Plasmids, Including Those EncodingVirB4/D4 Type IV Secretion Systems, on Salmonella enterica serovar Heidelberg Virulence in Macrophages and Epithelial Cells

Gokulan

Khare²,

Rooney³

et al. 2013

PLoS ONE

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Salmonella enterica serovar Heidelberg (S. Heidelberg) can cause foodborne illness in humans following the consumption of contaminated meat and poultry products. Recent studies from our laboratory have demonstrated that certain S. Heidelberg isolated from food-animal sources harbor multiple transmissible plasmids with genes that encode antimicrobial resistance, virulence and a VirB4/D4 type-IV secretion system. This study examines the potential role of these transmissible plasmids in bacterial uptake and survival in intestinal epithelial cells and macrophages, and the molecular basis of host immune system modulation that may be associated with disease progression. A series of transconjugant and transformant strains were developed with different combinations of the plasmids to determine the roles of the individual and combinations of plasmids on virulence. Overall the Salmonella strains containing the VirB/D4 T4SS plasmids entered and survived in epithelial cells and macrophages to a greater degree than those without the plasmid, even though they carried other plasmid types. During entry in macrophages, the VirB/D4 T4SS encoding genes are up-regulated in a time-dependent fashion. When the potential mechanisms for increased virulence were examined using an antibacterial Response PCR Array, the strain containing the T4SS down regulated several host innate immune response genes which likely contributed to the increased uptake and survival within macrophages and epithelial cells.

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Innate Humoral Defense Factors

Cited by 14 publications

References 222 publications

Lactoferrin increases both resistance to Salmonella typhimurium infection and the production of antibodies in mice

Lactoferrin increases both resistance to Salmonella typhimurium infection and the production of antibodies in mice

Nasal Colonization with Streptococcus pneumoniae Includes Subpopulations of Surface and Invasive Pneumococci

Impact of Plasmids, Including Those EncodingVirB4/D4 Type IV Secretion Systems, on Salmonella enterica serovar Heidelberg Virulence in Macrophages and Epithelial Cells

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