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Crosby, M. B., Zhang, J., Nowling, T. M., Svenson, J. L., Nicol, C. J., Gonzalez, F. J., et al. (2006). Inflammatory modulation of PPAR gamma expression and activity. Clin Immunol, 118(2-3), 276–283.
Abstract: Nitric oxide (NO) production increases with age in the lupus-prone MRL/lpr mouse, paralleling disease activity. One mechanism for excess NO production in MRL/lpr mice may be a defect in down-regulatory mechanisms of the iNOS pathway. A potential modulator of NO is the nuclear hormone receptor peroxisome proliferation activated receptor gamma (PPARgamma). We demonstrate that renal PPARgamma protein expression was altered as disease progressed in MRL/lpr mice, which paralleled increased iNOS protein expression. Additionally, MRL/lpr-derived primary mesangial cells expressed less PPARgamma than BALB/c mesangial cells and produced more NO in response to LPS and IFNgamma. Furthermore, PPARgamma activity was reduced in mesangial cells following exposure to inflammatory mediators. This activity was restored with the addition of a NOS enzyme inhibitor. These results indicate that the activation of inflammatory pathways may lead to reduced activity and expression of PPARgamma, further exacerbating the disease state.
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Dauphin, G., Zientara, S., Zeller, H., & Murgue, B. (2004). West Nile: worldwide current situation in animals and humans. Comp Immunol Microbiol Infect Dis, 27(5), 343–355.
Abstract: West Nile (WN) virus is a mosquito-borne flavivirus that is native to Africa, Europe, and Western Asia. It mainly circulates among birds, but can infect many species of mammals, as well as amphibians and reptiles. Epidemics can occur in rural as well as urban areas. Transmission of WN virus, sometimes involving significant mortality in humans and horses, has been documented at erratic intervals in many countries, but never in the New World until it appeared in New York City in 1999. During the next four summers it spread with incredible speed to large portions of 46 US states, and to Canada, Mexico, Central America and the Caribbean. In many respects, WN virus is an outstanding example of a zoonotic pathogen that has leaped geographical barriers and can cause severe disease in human and equine. In Europe, in the past two decades there have been a number of significant outbreaks in several countries. However, very little is known of the ecology and natural history of WN virus transmission in Europe and most WN outbreaks in humans and animals remain unpredictable and difficult to control.
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Nelson, D. M., Gardner, I. A., Chiles, R. F., Balasuriya, U. B., Eldridge, B. F., Scott, T. W., et al. (2004). Prevalence of antibodies against Saint Louis encephalitis and Jamestown Canyon viruses in California horses. Comp Immunol Microbiol Infect Dis, 27(3), 209–215.
Abstract: Jamestown Canyon (JC) and Saint Louis encephalitis (SLE) viruses are mosquito-transmitted viruses that have long been present in California. The objective of this study was to determine the seroprevalence of these two viruses in horses prior to the introduction of West Nile (WN) virus. Approximately 15% of serum samples collected in 1998 from 425 horses on 44 equine operations horses throughout California had serum antibodies to JC virus, whereas antibodies were not detected to SLE virus. The results indicate that horses in California were commonly infected prior to 1998 with mosquito-transmitted Bunyaviruses that are identical or closely related to JC virus, but not with SLE virus. The different seroprevalence of SLE and JC viruses in horses likely reflects the unique ecology of each virus, and it is predicted that WN virus will have a wider distribution in California than closely related SLE virus.
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Tumova, B. (1980). Equine influenza--a segment in influenza virus ecology. Comp Immunol Microbiol Infect Dis, 3(1-2), 45–59.
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Milouchine, V. N. (1980). The role of WHO in international studies on the ecology of influenza in animals. Comp Immunol Microbiol Infect Dis, 3(1-2), 25–31.
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Hall, R. A., Broom, A. K., Smith, D. W., & Mackenzie, J. S. (2002). The ecology and epidemiology of Kunjin virus. Curr Top Microbiol Immunol, 267, 253–269.
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Endy, T. P., & Nisalak, A. (2002). Japanese encephalitis virus: ecology and epidemiology. Curr Top Microbiol Immunol, 267, 11–48.
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Vaerman, J. P., Querinjean, P., & Heremans, J. F. (1971). Studies on the IgA System of the Horse. Immunol., (21), 443.
Abstract: Equine serum and secretions were found to contain a protein which
cross-reacted with an antiserum against human IgA, but not with antisera against
any other human immunoglobulin. The physicochemical properties of equint
IgA resembled those of human IgA. IgA was found to be the immunoglobulin
having the highest secretion vs serum concentration ratio in equine lacteal and salivary
secretions, and to be the protein produced by the majority of immunoglobulin-
containing cells in the lamina propria of the equine intestine.
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Shen, Y. - Q., Hebert, G., Lin, L. - Y., Luo, Y. - L., Moze, E., Li, K. - S., et al. (2005). Interleukine-1β and interleukine-6 levels in striatum and other brain structures after MPTP treatment: influence of behavioral lateralization. Journal of Neuroimmunology, 158(1–2), 14–25.
Abstract: MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induces diminution of the dopamine in nigrostriatal pathway and cognitive deficits in mice. MPTP treatment also increases pro-inflammatory cytokine production in substantia nigra and striatum. Since, pro-inflammatory cytokines influence striatal dopamine content and provoke cognitive impairments, the cognitive defects induced by MPTP may be partly due to brain cytokine induction in other structures than nigrostriatal pathway. Furthermore, behavioral lateralization, as assessed by paw preference, influences cytokine production at the periphery and in the central nervous system. Behavioral lateralization may thus influence brain cytokine levels after MPTP. In order to address these issues, mice selected for paw preference were injected with 25 mg/kg MPTP i.p. for five consecutive days after which striatal dopamine and DOPAC contents were measured by HPLC and IL-1β and IL-6 quantified by ELISA in the striatum, cerebral cortex, hippocampus and hypothalamus. The results showed that MPTP treatment induced dramatic loss of DA in striatum, simultaneously, IL-6 levels decreased in the striatum and increased in hippocampus and hypothalamus, while IL-1β levels decreased in the striatum, cerebral cortex and hippocampus. Interestingly, striatal dopamine turnover under basal conditions as well as striatal IL-1β and IL-6 levels under basal conditions and after MPTP depended on behavioral lateralization. Left pawed mice showed a higher decrease in dopamine turnover and lower cytokine levels as compared to right pawed animals. Behavioral lateralization also influenced IL-6 hippocampal levels under basal conditions and IL-1β cortical levels after MPTP. From these results, it can be concluded that MPTP-induced cognitive defects are accompanied by an alteration of pro-inflammatory cytokine levels in brain structures other than those involved in the nigrostriatal pathway. In addition, MPTP-induced dopamine decrease is influenced by behavioral lateralization, possibly through an effect on brain cytokine levels.
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Hieshima, K., Kawasaki, Y., Hanamoto, H., Nakayama, T., Nagakubo, D., Kanamaru, A., et al. (2004). CC Chemokine Ligands 25 and 28 Play Essential Roles in Intestinal Extravasation of IgA Antibody-Secreting Cells. The Journal of Immunology, 173(6), 3668–3675.
Abstract: CCL25 (also known as thymus-expressed chemokine) and CCL28 (also known as mucosae-associated epithelial chemokine) play important roles in mucosal immunity by recruiting IgA Ab-secreting cells (ASCs) into mucosal lamina propria. However, their exact roles in vivo still remain to be defined. In this study, we first demonstrated in mice that IgA ASCs in small intestine expressed CCR9, CCR10, and CXCR4 on the cell surface and migrated to their respective ligands CCL25, CCL28, and CXCL12 (also known as stromal cell-derived factor 1), whereas IgA ASCs in colon mainly expressed CCR10 and CXCR4 and migrated to CCL28 and CXCL12. Reciprocally, the epithelial cells of small intestine were immunologically positive for CCL25 and CCL28, whereas those of colon were positive for CCL28 and CXCL12. Furthermore, the venular endothelial cells in small intestine were positive for CCL25 and CCL28, whereas those in colon were positive for CCL28, suggesting their direct roles in extravasation of IgA ASCs. Consistently, in mice orally immunized with cholera toxin (CT), anti-CCL25 suppressed homing of CT-specific IgA ASCs into small intestine, whereas anti-CCL28 suppressed homing of CT-specific IgA ASCs into both small intestine and colon. Reciprocally, CT-specific ASCs and IgA titers in the blood were increased in mice treated with anti-CCL25 or anti-CCL28. Anti-CXCL12 had no such effects. Finally, both CCL25 and CCL28 were capable of enhancing α4 integrin-dependent adhesion of IgA ASCs to mucosal addressin cell adhesion molecule-1 and VCAM-1. Collectively, CCL25 and CCL28 play essential roles in intestinal homing of IgA ASCs primarily by mediating their extravasation into intestinal lamina propria.
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