Vasoactive Intestinal Peptide Balances Pro- and Anti-Inflammatory Cytokines in the <i>Pseudomonas aeruginosa</i>-Infected Cornea and Protects against Corneal Perforation

Szliter, Elizabeth A.; Lighvani, Shahrzad; Barrett, Ronald P.; Hazlett, Linda D.

doi:10.4049/jimmunol.178.2.1105

Cited by 67 publications

(77 citation statements)

References 34 publications

(37 reference statements)

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“…2,33,36 Briefly, M were induced into the peritoneal cavity by intraperitoneal injection of 1 mL of 3% Brewer's thioglycollate medium (BD Biosciences, Sparks, MD) 5 days before kill. Cells were collected by peritoneal lavage with DMEM containing 10% FBS and stained with 0.4% trypan blue, and viable cells (Ͼ95%) were counted with a hemacytometer.…”

Section: Isolation and Stimulation To Detect St2 By Rt-pcrmentioning

confidence: 99%

IL-33 Shifts Macrophage Polarization, Promoting Resistance againstPseudomonas aeruginosaKeratitis

Hazlett

McClellan

Barrett

et al. 2010

Invest. Ophthalmol. Vis. Sci.

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Section: Isolation and Stimulation To Detect St2 By Rt-pcrmentioning

confidence: 99%

IL-33 Shifts Macrophage Polarization, Promoting Resistance againstPseudomonas aeruginosaKeratitis

Hazlett

McClellan

Barrett

et al. 2010

Invest. Ophthalmol. Vis. Sci.

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“…Control sections were similarly treated but without primary Ab application. Sections were visualized and digital images were captured with a confocal laser scanning microscope (TSC SP2; Leica Microsystems) (31). Stimulated peritoneal M (described above) were fixed for 10 min with 3.7% formaldehyde.…”

Section: Nkt Nk and M Cell Immunolabelingmentioning

confidence: 99%

NKT Cells Are Critical to Initiate an Inflammatory Response after Pseudomonas aeruginosa Ocular Infection in Susceptible Mice

Hazlett

Liu

et al. 2007

The Journal of Immunology

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CD4+ T cells produce IFN-γ contributing to corneal perforation in C57BL/6 (B6) mice after Pseudomonas aeruginosa infection. To determine the role of NK and NKT cells, infected corneas of B6 mice were dual immunolabeled. Initially, more NKT than NK cells were detected, but as disease progressed, NK cells increased, while NKT cells decreased. Therefore, B6 mice were depleted of NK/NKT cells with anti-asialo GM1 or anti-NK1.1 Ab. Either treatment accelerated time to perforation, increased bacterial load and polymorphonuclear neutrophils, but decreased IFN-γ and IL-12p40 mRNA expression vs controls. Next, RAG-1 knockout (−/−; no T/NKT cells), B6.TCR Jα281−/− (NKT cell deficient), α-galactosylceramide (αGalCer) (anergized NKT cells) injected and IL-12p40−/− vs B6 controls were tested. IFN-γ mRNA was undetectable in RAG-1−/−- and αGalCer-treated mice at 5 h and was significantly reduced vs controls at 1 day postinfection. It also was reduced significantly in B6.TCR Jα281−/−, αGalCer-treated, and IL-12p40−/− (activated CD4+ T cells also reduced) vs control mice at 5 days postinfection. In vitro studies tested whether endotoxin (LPS) stimulated Langerhans cells and macrophages (Mφ; from B6 mice) provided signals to activate NKT cells. LPS up-regulated mRNA expression for IL-12p40, costimulatory molecules CD80 and CD86, NF-κB, and CD1d, and addition of rIFN-γ potentiated Mφ CD1d levels. Together, these data suggest that Langerhans cell/Mφ recognition of microbial LPS regulates IL-12p40 (and CD1d) driven IFN-γ production by NKT cells, that IFN-γ is required to optimally activate NK cells to produce IFN-γ, and that depletion of both NKT/NK cells results in earlier corneal perforation.

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“…Any of these conditions could play a more dominant role in BALB/C than in B6 mice. Such differences in immune responses between B6 and BALB/C are not unusual, especially with regard to cytokine responses [37,38,39], and explanations have not always been straightforward [40,41]. …”

Section: Discussionmentioning

confidence: 99%

Enhancement of Antigen-Specific Immunoglobulin G Responses by Anti-CD48

Yuan¹,

Guo²,

Thet³

2012

J Innate Immun

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CD48 is a glycosylphosphatidylinositol-anchored protein expressed ubiquitously on many cell types. Despite the poor ability to signal on its own, CD48 can activate cells via interaction with its counter receptors CD2 and CD244 as well as influence the function of other cell surface molecules by costimulatory activities. We show, herein, that injection of anti-CD48 antibodies into mice can augment the antibody response to a T-independent antigen, NP-Ficoll, that is representative of antigenic determinants expressed on the surface of various pathogens, such as Streptococcus pneumoniae. In C57BL/6 mice, enhancement of the response is dependent on natural killer (NK) cells as well as on the presence of CD2 and CD244, ligands for CD48, suggesting a requirement for direct interaction between NK and B cells. Interestingly, in this case, despite a similar augmentation by anti-CD48 in BALB/C mice, the response is independent of NK or T cells, suggesting that help for this response can be derived from other innate cell types. These results provide a pathway by which CD48, when appropriately activated, can influence the course of an antigen-specific antibody response via the innate system.

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Vasoactive Intestinal Peptide Balances Pro- and Anti-Inflammatory Cytokines in the Pseudomonas aeruginosa-Infected Cornea and Protects against Corneal Perforation

Cited by 67 publications

References 34 publications

IL-33 Shifts Macrophage Polarization, Promoting Resistance againstPseudomonas aeruginosaKeratitis

IL-33 Shifts Macrophage Polarization, Promoting Resistance againstPseudomonas aeruginosaKeratitis

NKT Cells Are Critical to Initiate an Inflammatory Response after Pseudomonas aeruginosa Ocular Infection in Susceptible Mice

Enhancement of Antigen-Specific Immunoglobulin G Responses by Anti-CD48

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