• Journal of Veterinary Science
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• v.22 no.2
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• pp.20.1-20.13
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• 2021

Background: Pseudorabies virus (PRV) infection leads to high mortality in swine. Despite extensive efforts, effective treatments against PRV infection are limited. Furthermore, the inflammatory response induced by PRV strain GXLB-2013 is unclear. Objectives: Our study aimed to investigate the inflammatory response induced by PRV strain GXLB-2013, establish an inflammation model to elucidate the pathogenesis of PRV infection further, and develop effective drugs against PRV infection. Methods: Kunming mice were infected intramuscularly with medium, LPS, and different doses of PRV-GXLB-2013. Viral spread and histopathological damage to brain, spleen, and lung were determined at 7 days post-infection (dpi). Immune organ indices, levels of reactive oxygen species (ROS), nitric oxide (NO), and inflammatory cytokines, as well as levels of activity of COX-2 and iNOS were determined at 4, 7, and 14 dpi. Results: At 10⁵-10⁶ TCID₅₀ PRV produced obviously neurological symptoms and 100% mortality in mice. Viral antigens were detectable in kidney, heart, lung, liver, spleen, and brain. In addition, inflammatory injuries were apparent in brain, spleen, and lung of PRV-infected mice. Moreover, PRV induced increases in immune organ indices, ROS and NO levels, activity of COX-2 and iNOS, and the content of key pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, interferon-γ and MCP-1. Among the tested doses, 10² TCID₅₀ of PRV produced a significant inflammatory mediator increase. Conclusions: An inflammatory model induced by PRV infection was established in mice, and 10² TCID50 PRV was considered as the best concentration for the establishment of the model.

• Journal of Microbiology and Biotechnology
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• v.20 no.11
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• pp.1585-1591
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• 2010

A comprehensive study on the production of inflammatory mediators in the lungs of BALB/c mice following infection with Stenotrophomonas maltophilia was conducted. The levels of pro-inflammatory cytokines, tumor necrosis factor alpha (TNF-${\alpha}$), and interleukin-1${\beta}$ (IL-1${\beta}$) were raised in the lungs of infected mice compared with control. The production of anti-inflammatory cytokine IL-10 was slightly delayed. Its peak level was on the $2^{nd}$ day, whereas the peak of pro-inflammatory cytokines was observed on day 1 after intranasal challenge. This was accompanied by a rise in myeloperoxidase (MPO) and malondialdehyde (MDA) on day 1. The increase in MPO levels matched with histopathological observations, as neutrophils infiltration was detected on the first day. Alveolar macrophages (AMs) obtained from infected animals showed a higher rate of uptake and killing when exposed to bacteria in vitro, compared with similar experiments conducted with AMs from normal mice (control). This suggests that AMs were more efficient in cleaning the bacteria. The nitric oxide (NO) production however started early during infection but reached its maximum on the $3^{rd}$ day. No mortality was observed among the infected animals, and infection was resolved by the $5^{th}$ day post infection. No drastic changes in the lung tissue were observed on histopathological examination.

• Journal of Korean Neurosurgical Society
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• v.38 no.3
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• pp.206-210
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• 2005

Objective : Our aim is to evaluate the early changes of biologic markers such as white blood cell[WBC] count, erythrocyte sedimentation rate[ESR] and C-reactive protein[CRP] in early diagnosis of postoperative infection and to differentiate infection from inflammatory reaction in lumbar spine surgery. Methods : We reviewed 330patients who had undergone spinal operations between May 1999 and October 2001. For this study, the patients were classified into two groups, which include a group that underwent spinal decompressive surgery without instrumentation[SD], and the other group that underwent fusion surgery with spinal instrumentation[SI]. And each group was also subdivided into two groups respectively, one with infection and the other without infection. We retrospectively analyzed the WBC count, ESR and CRP preoperatively and postoperatively, according to their operation type and postoperative infection history. Results : Inflammatory indices were physiologically affected by instrumentation itself. But ESR and CRP elevations were more prolonged and sustained under infection. In SD patients without infection, ESR and CRP were stabilized 5 days after surgery. In SI patients without infection, CRP was stabilized about 7days after surgery, but ESR showed sustained and variously elevated. In both SD and SI groups, the stabilization of CRP was the most reliable behavior of surgery without infection. Conclusion : C-reactive protein is most sensitive parameter for postoperative spine infection. The knowledge of the inflammatory indices and their relatively uniform patterns with or without infection offers surgeons the ability to infer the state of surgical wound.

• Parasites, Hosts and Diseases
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• v.61 no.1
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• pp.2-14
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• 2023

Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic T. vaginalis infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between T. vaginalis infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of T. vaginalis in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of T. vaginalis trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. T. vaginalis also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, T. vaginalis is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by T. vaginalis-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal-epithelial interaction, suggesting that the proliferation of T. vaginalis-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that T. vaginalis contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.

• Journal of Microbiology
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• v.41 no.3
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• pp.266-270
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• 2003

Orientia tsutsugamushi, an obligate intracellular bacterium, is the causative agent of scrub typhus which is histopathologically characterized by inflammatory manifestations. To understand the pathogenesis of scrub typhus, chemokine gene expression in mice after infection with O. tsutsugamushi was investigated. The mRNAs that were upregulated included macrophage inflammatory proteins 1${\alpha}$/${\beta}$ (MIP-1${\alpha}$/${\beta}$), MIP-2, monocyte chemoattractant protein 1, RANTES (regulated upon activation, normal T-cell expressed and secreted), and gamma-interferon-inducible protein 10. Peak expression of these chemokines was observed six days after infection. These responses returned to or approached baseline preinfection levels by eight days after infection. Chemokine profiles in infected mice were well correlated with the kinetics of inflammatory cell infiltration. Thus, O. tsutsugamushi appears to be a strong inducer of chemokines which may significantly contribute to the inflammation observed in scrub typhus by attracting and activating phagocytic leukocytes.

• Annals of Clinical Neurophysiology
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• v.19 no.1
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• pp.50-53
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• 2017

An infection is less likely to elicit chronic inflammatory demyelinating polyneuropathy (CIDP) than Guillain-$Barr{\acute{e}}$ syndrome. We here report a case of acute-onset CIDP following hepatitis A virus infection and briefly comment on the potential mechanisms regarding the induction and chronicity of autoimmunity after a viral infection.

• Annals of Clinical Neurophysiology
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• v.13 no.2
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• pp.97-100
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• 2011

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated polyneuropathy. Corticosteroids, intravenous immunoglobulin (IVIG) and plasmapheresis have been reported to be effective treatment. Rarely, CIDP can occur in the patients with HIV infection. The clinical features and electrophysiological findings of CIDP are known to be similar in patients with and without HIV infection. We report a 30-year-old male with HIV infection associated CIDP who improved after the administration of intravenous immunoglobulin and long term oral prednisone.

• IMMUNE NETWORK
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• v.14 no.3
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• pp.123-127
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• 2014

Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as tumor necrosis factor-${\alpha}(TNF{\alpha})$ and IL-6 and its expression is elevated in various inflammatory autoimmune diseases, certain cancers, as well as viral infections. IL-32 gene was first cloned from activated T cells, however IL-32 expression was also found in other immune cells and non-immune cells. IL-32 gene was identified in most mammals except rodents. It is transcribed as multiple-spliced variants in the absence of a specific activity of each isoform. IL-32 has been studied mostly in clinical fields such as infection, autoimmune, cancer, vascular disease, and pulmonary diseases. It is difficult to investigate the precise role of IL-32 in vivo due to the absence of IL-32 gene in mouse. The lack of mouse IL-32 gene restricts in vivo studies and restrains further development of IL-32 research in clinical applications although IL-32 new cytokine getting a spotlight as an immune regulatory molecule processing important roles in autoimmune, infection, and cancer. In this review, we discuss the regulation and function of IL-32 in inflammatory bowel diseases and rheumatoid arthritis.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.17 no.2
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• pp.1-11
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• 2004

Objective: Chronic otitis media is an inflammation and infection of the middle ear which is persistent. Chronic otitis media occurs when the eustachian tube becomes blocked repeatedly, multiple infections, ear trauma, or swelling of the adenoids. A chronic ear may be the result of an acute ear infection that does not clear completely, or the result of recurrent ear infections. A chronic ear infection may be more destructive than an acute ear infection because its effects are prolonged, and it may cause permanent damage to the ear. Methods : Experimental animals made use of 4-5 weeks age(weight 20-25g) ICR(male)mouse. In the breeding farm, the lighting time was controlled from 7:00 am until 7:00 pm, the temperature was controlled within $22{\pm}0.5{\circ}$ and water and food were not limited. The extracts which were extracted from Hwangginaetak-san devided low dose group( 1.0g/kg-HN) and high dose group(3.0g/kg-HN), they were intragastrically administered to the mouse of sample A and sample B prior to LPS I.P injection. Compared with inflammation induced group which were induced by LPS, we measured the WBC count, IL-6 level in plasma and TNF-${\alpha}$ level in plasma. Results: 1. Hwangginaetak-san decreased WBC count in inflammatory reaction induced by LPS 2. Hwangginaetak-san decreased IL-6 level in inflammatory reaction induced by LPS. 3. Hwangginaetak-san didn't decreased TNF-${\alpha}$ level in inflammatory reaction induced by LPS Conclusion: According to above results, Hwangginaetak-san was improved its suppression effect to the inflammatory reaction through WBC count and IL-6 level. So Hwangginaetak-san is considered to be used for treatment of chronic otitis media by controlling the WBC count and IL-6 level in plasma.

• IMMUNE NETWORK
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• v.21 no.2
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• pp.13.1-13.19
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• 2021

Macrophages are important for the first line of defense against microbial pathogens. Integrin CD11b, which is encoded by Itgam, is expressed on the surface of macrophages and has been implicated in adhesion, migration, and cell-mediated cytotoxicity. However, the functional impact of CD11b on the inflammatory responses of macrophages upon microbial infection remains unclear. Here, we show that CD11b deficiency resulted in increased susceptibility to sepsis induced by methicillin-resistant Staphylococcus aureus (MRSA) infection by enhancing the pro-inflammatory activities of macrophages. Upon infection with MRSA, the mortality of Itgam knockout mice was significantly higher than that of control mice, which is associated with increased production of TNF-α and IL-6. In response to MRSA, both bone marrow-derived macrophages and peritoneal macrophages lacking CD11b produced elevated amounts of pro-inflammatory cytokines and nitric oxide. Moreover, CD11b deficiency upregulated IL-4-induced expression of anti-inflammatory mediators such as IL-10 and arginase-1, and an immunomodulatory function of macrophages to restrain T cell activation. Biochemical and confocal microscopy data revealed that CD11b deficiency augmented the activation of NF-κB signaling and phosphorylation of Akt, which promotes the functional activation of macrophages with pro-inflammatory and immunoregulatory phenotypes, respectively. Overall, our experimental evidence suggests that CD11b is a critical modulator of macrophages in response to microbial infection.