scholarly journals Macrophage inflammatory protein 3α deficiency in atopic dermatitis skin and role in innate immune response to vaccinia virus

2007 ◽  
Vol 119 (2) ◽  
pp. 457-463 ◽  
Author(s):  
Byung Eui Kim ◽  
Donald Y.M. Leung ◽  
Joanne E. Streib ◽  
Mark Boguniewicz ◽  
Qutayba A. Hamid ◽  
...  
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Vaccinia Virus ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

scholarly journals Cytokine Milieu of Atopic Dermatitis Skin Subverts the Innate Immune Response to Vaccinia Virus

Immunity ◽  
2006 ◽  
Vol 24 (3) ◽  
pp. 341-348 ◽  
Author(s):  
Michael D. Howell ◽  
Richard L. Gallo ◽  
Mark Boguniewicz ◽  
James F. Jones ◽  
Cathy Wong ◽  
...  
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Vaccinia Virus ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Cytokine Milieu

scholarly journals Promotion of Colonization and Virulence by Cholera Toxin Is Dependent on Neutrophils

2013 ◽  
Vol 81 (9) ◽  
pp. 3338-3345 ◽  
Author(s):  
Jessica Queen ◽  
Karla J. F. Satchell
Keyword(s):  
Immune Response ◽  
Cholera Toxin ◽  
Innate Immune Response ◽  
Host Response ◽  
Survival Rates ◽  
Innate Immune ◽  
Infection Model ◽  
High Dose ◽  
Content Type ◽  
Inflammatory Protein

ABSTRACTThe innate immune response toVibrio choleraeinfection is poorly understood, but this knowledge is critical for the design of safe, effective vaccines. Using an adult mouse intestinal infection model, this study examines the contribution of neutrophils to host immunity, as well as the effect of cholera toxin and other secreted factors on this response. Depletion of neutrophils from mice with anti-Ly6G IA8 monoclonal antibody led to similar survival rates of mice infected with low or moderate doses of toxigenicV. choleraeEl Tor O1. At a high dose, neutropenic mice showed increased rates of survival compared to neutrophil-replete animals. Expression of cholera toxin was found to be protective to the neutropenic host, and this phenotype can be replicated by the administration of purified toxin. Neutrophils do not effectively clear colonizing bacteria from the small intestine, nor do they alter induction of early immune-modulating signals. In both neutropenic and neutrophil-replete animals, the local response to infection is characterized by expression of interleukin 6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha (MIP-2). Overall, these data indicate that the innate immune response to toxigenicV. choleraeinfection differs dramatically from the host response to nontoxigenic infection or vaccination, where neutrophils are protective to the host. In the absence of neutrophils, cholera toxin induces immunomodulatory effects that increase host survival. In cholera toxin-producing strains, similar to nontoxigenic infection, accessory toxins are critical to virulence, indicating that cholera toxin and the other secreted toxins modulate the host response by different mechanisms, with both contributing to bacterial persistence and virulence.

scholarly journals Vaccinia Virus Subverts a Mitochondrial Antiviral Signaling Protein-Dependent Innate Immune Response in Keratinocytes through Its Double-Stranded RNA Binding Protein, E3

2008 ◽  
Vol 82 (21) ◽  
pp. 10735-10746 ◽  
Author(s):  
Liang Deng ◽  
Peihong Dai ◽  
Tanvi Parikh ◽  
Hua Cao ◽  
Vijay Bhoj ◽  
...  
Keyword(s):  
Immune Response ◽  
Vaccinia Virus ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Antiviral Signaling ◽  
Double Stranded Rna ◽  
Signaling Protein ◽  
Dsrna Binding ◽  
Mitochondrial Antiviral Signaling ◽  
Mitochondrial Antiviral Signaling Protein

ABSTRACT Skin keratinocytes provide a first line of defense against invading microorganisms in two ways: (i) by acting as a physical barrier to pathogen entry and (ii) by initiating a vigorous innate immune response upon sensing danger signals. How keratinocytes detect virus infections and generate antiviral immune responses is not well understood. Orthopoxviruses are dermatotropic DNA viruses that cause lethal disease in humans. Virulence in animal models depends on the virus-encoded bifunctional Z-DNA/double-stranded RNA (dsRNA)-binding protein E3. Here, we report that infection of mouse primary keratinocytes with a vaccinia ΔE3L mutant virus triggers the production of beta interferon (IFN-β), interleukin-6 (IL-6), CCL4, and CCL5. None of these immune mediators is produced by keratinocytes infected with wild-type vaccinia virus. The dsRNA-binding domain of E3 suffices to prevent activation of the innate immune response. ΔE3L induction of IFN-β, IL-6, CCL4, and CCL5 secretion requires mitochondrial antiviral signaling protein (MAVS; an adaptor for the cytoplasmic viral RNA sensors RIG-I and MDA5) and the transcription factor IRF3. IRF3 phosphorylation is induced in keratinocytes infected with ΔE3L, an event that depends on MAVS. The response of keratinocytes to ΔE3L is unaffected by genetic ablation of Toll-like receptor 3 (TLR3), TRIF, TLR9, and MyD88.

scholarly journals Vaccinia virus immune evasion: mechanisms, virulence and immunogenicity

2013 ◽  
Vol 94 (11) ◽  
pp. 2367-2392 ◽  
Author(s):  
Geoffrey L. Smith ◽  
Camilla T. O. Benfield ◽  
Carlos Maluquer de Motes ◽  
Michela Mazzon ◽  
Stuart W. J. Ember ◽  
...  
Keyword(s):  
Immune Response ◽  
Vaccinia Virus ◽  
Innate Immune Response ◽  
Immune Evasion ◽  
Mammalian Cells ◽  
Innate Immune ◽  
Gene Encoding ◽  
Cytokines And Chemokines ◽  
Host Innate Immune Response ◽  
New Hosts

Virus infection of mammalian cells is sensed by pattern recognition receptors and leads to an innate immune response that restricts virus replication and induces adaptive immunity. In response, viruses have evolved many countermeasures that enable them to replicate and be transmitted to new hosts, despite the host innate immune response. Poxviruses, such as vaccinia virus (VACV), have large DNA genomes and encode many proteins that are dedicated to host immune evasion. Some of these proteins are secreted from the infected cell, where they bind and neutralize complement factors, interferons, cytokines and chemokines. Other VACV proteins function inside cells to inhibit apoptosis or signalling pathways that lead to the production of interferons and pro-inflammatory cytokines and chemokines. In this review, these VACV immunomodulatory proteins are described and the potential to create more immunogenic VACV strains by manipulation of the gene encoding these proteins is discussed.

scholarly journals Staphylococcus pseudintermedius, both commensal and pathogen

2018 ◽  
Vol 74 (1) ◽  
pp. 6042-2018
Author(s):  
Dorota Chrobak-Chmiel ◽  
Anna Golke ◽  
Kourou Dembele ◽  
Katarzyna Ćwiek ◽  
Magdalena Kizerwetter-Świda ◽  
...  
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Immune System ◽  
Virulence Factors ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Staphylococcus Pseudintermedius ◽  
Underlying Condition ◽  
Secondary Infections ◽  
Pathogenic Effects

Staphylococcus pseudintermedius is considered to be a both commensal and opportunistic canine pathogen. The anal, perineal and nasal locations appear to be the main S. pseudintermedius colonization sites, from which bacteria are transmitted to other body sites, causing secondary infections. When the immune system is compromised because of an underlying condition, the skin becomes susceptible to infection. Thus, the host’s condition seems to play a crucial role in the pathogenesis of S. pseudintermedius infections. There are some predisposing factors, one of which is atopic dermatitis. The pathogenic effects of S. pseudintermedius are mediated by several virulence factors, for instance superantigens, which play an important role by causing dermatitis. The immune system has evolved many different mechanisms to recognize and deal with pathogens, but bacteria have also developed various strategies to evade them. In this review, we focus on early stages of the innate immune response with particular emphasis on the mechanisms of recognition of staphylococci and the action of antimicrobial peptides. .

Suppression of innate immune response genes in the skin of atopic dermatitis (AD)

2003 ◽  
Vol 111 (2) ◽  
pp. S272
Author(s):  
I. Nomura ◽  
P.Y. Ong ◽  
E. Goleva ◽  
M. Boguniewicz ◽  
C. Hall ◽  
...  
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Immune Response Genes

The cutaneous innate immune response in patients with atopic dermatitis

2013 ◽  
Vol 131 (2) ◽  
pp. 266-278 ◽  
Author(s):  
I-Hsin Kuo ◽  
Takeshi Yoshida ◽  
Anna De Benedetto ◽  
Lisa A. Beck
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Innate Immune Response ◽  
Innate Immune

scholarly journals Cytokine Milieu of Atopic Dermatitis, as Compared to Psoriasis, Skin Prevents Induction of Innate Immune Response Genes

2003 ◽  
Vol 171 (6) ◽  
pp. 3262-3269 ◽  
Author(s):  
Ichiro Nomura ◽  
Elena Goleva ◽  
Michael D. Howell ◽  
Quatyba A. Hamid ◽  
Peck Y. Ong ◽  
...  
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Immune Response Genes ◽  
Cytokine Milieu
Sign in / Sign up

Export Citation Format

Share Document