Chikungunya fever: General and oral healthcare implications.

Chikungunya virus (CHIKV) was first isolated in humans in 1952, following an epidemic in Tanzania. The origin of the name means "to bend forward or become contorted," in reference to the posture adopted by patients due to the joint pain that occurs during the infection. Epidemiology data suggest that by the end of 2015, about 1.6 million people had been infected with CHIKV. The acute period of the disease is characterized by high fever, myalgia, joint pain, and severe and disabling polyarthritis, sometimes accompanied by headache, backache, and maculopapular rash, predominantly on the thorax. Around half of the patients will progress to the subacute and chronic phases, that is manifested by persistent polyarthritis/polyarthralgia, accompanied by morning stiffness and fatigue, which could remain for years. Oral features may include gingivitis possibly as a consequence of arthralgia of the hands leading to limited oral health measures as well as burning sensation and oral mucosal ulceration. Treatment in the acute phase includes acetaminophen, and weak opioids (tramadol or codeine) should be used in cases of severe or refractory pain. For patients who have progressed to the subacute stage and who have not had notable benefit from common analgesics or opioids, NSAIDs, or adjunctive pain medications (anticonvulsants or antidepressants) may be of benefit. In patients with moderate-to-severe musculoskeletal pain or in those who cannot be given or tolerate NSIADs or opiates, prednisolone should be prescribed.

Immunomodulatory and therapeutic potential of a mucin-specific mycelial lectin from Aspergillus panamensis.

The present study reports the evaluation of immunomodulatory and therapeutic potential of a purified Aspergillus panamensis lectin. The immunomodulatory potential of the purified lectin was determined in swiss albino mice by studying its effect on anaphylaxis reaction, arthus reaction, respiratory burst activity, nitric oxide production and quantification of cytokine levels. The therapeutic potential of the lectin was evaluated in male wistar rat models by studying its curative effect on ulcerative colitis. The purified lectin inhibited systemic anaphylaxis and arthus reaction. It enhanced the functional ability of macrophages which was evident from increase in reduction of nitroblue tetrazolium dye and nitric oxide production. It also stimulated the production of Th-1 cytokine IFN-γ and Th-2 cytokine IL-6. Maximum immunomodulatory effect was seen at lectin concentration of 1.5mg/kg body weight. The lectin also showed curative effect against trinitrobenzene sulphonic acid induced ulcerative colitis. The results of this study adequately reflect the role of purified A. panamensis lectin in improving the immune status of mice models. They also show the effect of lectin in reducing the severity of incidence and decrease in clinical symptoms of ulcerative colitis.

Migration inhibitory factor (MIF) released by macrophages upon recognition of immune complexes is critical to inflammation in Arthus reaction.

Deposition of immune complexes (IC) triggers Fc gamma R-dependent inflammation, leading to tissue damage in rheumatoid arthritis, systemic lupus erythematous, immune glomerulonephritis, and several immune vasculitides. Evidences support a role for macrophage migration inhibitory factor (MIF) in a number of inflammatory diseases, but the triggering of its secretion and its physiopathological role upon IC deposition remain elusive. Herein, we show that human macrophages secreted MIF after IC recognition, which in turn controlled the secretion of TNF. Macrophages from Mif-/- mice produced smaller amounts of TNF when stimulated with IgG-opsonized erythrocytes than wild-type (WT) cells. Using passive reverse Arthus reaction in the peritoneum and lungs as a model for IC-induced inflammation, we demonstrated that Mif-/- mice had a milder response, observed by reduced neutrophil recruitment, vascular leakage, and secretion of TNF, MIP-2, and keratinocyte-derived chemokine compared with WT controls. Adoptive transfer of alveolar macrophages from WT to Mif-/- mice rescued pulmonary neutrophil recruitment and TNF production upon passive reverse Arthus reaction. Our study indicates that Arthus inflammatory reaction is largely dependent on MIF and poses macrophages as a source of the MIF released upon IC recognition. These results give experimental support to the proposition that blockade of MIF might constitute an adjunctive, therapeutic approach to IC disease.

Association of endothelin with lung hemorrhage induced by immune complexes in rats.

The participation of endothelins (ETs) in a model of neutrophil-dependent lung injury induced by intrabronchial instillation of rabbit antibodies to ovalbumin followed by i.v. injection of the antigens (Arthus reaction) was investigated. Hemorrhagic lesions were evaluated by measuring the extravasations of hemoglobin in lung parenchyma. From 5 min to 24 h after the Arthus reaction (AR), endothelin (ir-ET) levels in bronchoalveolar lavage fluid (BALF) and in plasma were measured by radioimmunoassay. BALF levels of ir-ET were not different between control and AR animals for the first 90 min after the antigen challenge but increased from 2 to 24 h after induction of AR. ET levels in the plasma did not change from the respective controls over the same 24 h period. Increased ir-ET in BALF was not affected by pretreatment with L-NAME (30 mg/kg, i.v.). A PAF antagonist (BN52021; 5 and 10 mg/kg, i.v.) increased ET content in BALF and decreased the intensity of the AR. Thiorphan (2 mg/kg, i.v.) inhibited the AR-induced hemorrhagic lesions in lungs. An ET(A) receptor antagonist, BQ-123 (1 mg/kg, i.v.) potentiated, whereas the ET(B) antagonist, BQ-788 (1 mg/kg, i.v.) inhibited the lung hemorrhage. It is concluded that ETs are released during and play a role in the lung AR.

Platelet-activating factor and eicosanoids are mediators of local and systemic changes induced by immune-complexes in mice.

A passive Arthus reaction (AR) induced in the peritoneal cavity of mice was followed by increased local vascular permeability and haemoconcentration. The intensity of the increased vasopermeability was higher in BALB/c compared with C3H/HePas mice despite the latter being 10 times more sensitive to platelet-activating factor (PAF). C3H/HePas mice however, exhibited higher levels of haemoconcentration and shock-like symptoms. Both events were inhibited by the PAF antagonist, WEB 2170. Indomethacin reduced both pathological events whereas L663,536, that inhibits leukotrienes synthesis reduced haemoconcentration but only in BALB/c mice. PAF was released into the peritoneal cavity, peak release being at 10 min after induction of AR. Prostaglandin E2 (PGE2), thromboxane B2 (TXB2), leukotriene B4 (LTB4), and leukotriene C4/D4 (LTC4/D4) were also released at this time. Similar levels of PAF and eicosanoids were found in BALB/c and C3H/HePas mice except for LTB4, which was higher in C3H/HePas. It is concluded that PAF and eicosanoids are mediators of local and systemic changes induced by immune complexes in the peritoneal cavity of mice.

Modulation by lipid mediators of immune complex-induced lung inflammation in mice.

The present study characterized a murine model of immune complex-induced pneumonitis and investigated the role of platelet-activating factor (PAF) and eicosanoids as mediators of lung neutrophil infiltration and hemorrhagic lesions. Rabbit antibodies to bovine serum albumin were injected into the airways and bovine serum albumin was injected intravenously into C3H/HePas and BALB/c mice. After 24 h, a significant increase in neutrophil infiltration and hemoglobin concentration in the bronchoalveolar lavage fluid and lung parenchyma was observed in both strains despite the C3H/HePas strain being 10 times more sensitive to PAF. Neutrophil influx and vascular lesions were not affected by pre-treatment of the mice with the PAF receptor antagonist, WEB 2170 (5-(2-chlorphenyl)carbonyl)-3,4-dihydro- 10-methyl-3-((4-morpholinyl)-2H,7H-cyclopenta(4,5)thieno(3,2-f)(1,2,4)-t riazolo-(4,3-a)(1,4)-diazepine). In contrast, neutrophil influx and vascular lesions were increased by the cyclo-oxygenase inhibitor, indomethacin, and reduced by the inhibitor of leukotriene synthesis, MK 886 (3-[1-(4-chlorobenzyl-3-t-butyl-thio-t-isopropyl-indol-2y-1]-2-2-+ ++dimethylpropanoic acid) and by the leukotriene B4 receptor antagonist, RO 0254094 (2-[(5-carboxypentyl)-6-[6-[3,4-dihidro-4-oxo-8-propyl-2H-1-benzop yran-7-yl)hexyl] benzenepropanoic acid). Increased levels of leukotriene B4, leukotriene C4/D4, thromboxane B2 were found in bronchoalveolar lavage fluid 4 h after induction of the reaction. There is also a tendency to increased prostaglandins E2 levels. Neutrophil infiltration and vascular lesions in immune complex-induced pneumonitis in mice are mediated by leukotriene B4.

Respuesta inmunologica del conejo ante la aplicacion de una solucion subfarmacologica de un antigeno micobacteriano / Immunological response of rabit by application of subpharmacological solution of mycobacterian antigen

Un antigeno micobacteriano se administro a conejos de la raza Nueva Zelanda, via agua para beber, en dosis subfarmacologicas: 1CH, 6CH, 12CH, 15CH y 30CH. Para evaluar la respuesta inmunologica se determino... (AU)

PAF modulates eicosanoids and TNF release in immune-complex arthritis in rats.

The participation of lipid mediators and tumor necrosis factor (TNF) on an experimental model of immune-complex arthritis was investigated. Male Wistar rats received intraarticular injection of rabbit antibodies to bovine serum albumin into the knee joint followed by i.v. injection of the antigen. The levels of eicosanoids and TNF released into the synovial exudates were then assessed using ELISA and the L929 lytic cell assay, respectively. Increase in the levels of LTB4, TXB2 and PGE2 were detected 5 min, 5 min, and 6 h after arthritis induction, respectively. Pretreatment with the PAF receptor antagonist WEB 2170 decreased the levels of PGE2 and increased those of LTB4, without altering TXB2 levels. Increase in the levels of TNF was detected at 3 h of arthritis. Pretreatment with either the cycloxygenase inhibitor indomethacin or the 5-lipoxygenase inhibitor L-663,536 had no effect on TNF levels. Pretreatment with WEB 2170 significantly decreased TNF levels. These results are the first demonstration of eicosanoids and TNF release in immune-complex arthritis. The data also suggest that PAF had both a positive and negative modulatory role on the release of PGE2 and LTB4, respectively. Moreover, TNF release into the synovial exudate did not depend on eicosanoids whereas platelet activating factor (PAF) appeared to mediate the release of this cytokine in the model.

Granuloma facial: Hallazgos de inmunofluorescencia directa en cuatro casos / Facial Granuloma

El granuloma facial es una entidad clínica e histológica bien definida, cuya etiología permanece desconocida. Los hallazgos por inmunofluorescencia directa de depósitos de inmunoglobulinas y complemento en las lesiones, inician un nuevo camino de investigación que aún no ha sido bien aclarado, ya que se alternan estudios positivos con otros megativos. Estudiamos 4 pacientes, 3 hombres y una mujer, con un rango de edad de 33 a 55 años; el tiempo de evolución de la enfermedad osciló entre 1 y 14 años. Todos los pacientes tenían compromiso facial. Uno presentó lesiones múltiples y otro se acompañaba de lesiones extrafaciales. La inmunofluorescencia directa fue positiva en dos casos, hallando depósitos granulares de IgA en zona de membrana basal. La IgG, IgM, IgE y complemento fueron negativos en los 4 casos. Las distintas características de las inmunoglobulinas más un factor ambiental (rayos ultravioletas) u otro, llevaría a la IgA de la circulación a los tejidos. Posteriormente lo haría la IgG en la respuesta secundaria

Granuloma facial: Hallazgos de inmunofluorescencia directa en cuatro casos / Facial Granuloma

El granuloma facial es una entidad clínica e histológica bien definida, cuya etiología permanece desconocida. Los hallazgos por inmunofluorescencia directa de depósitos de inmunoglobulinas y complemento en las lesiones, inician un nuevo camino de investigación que aún no ha sido bien aclarado, ya que se alternan estudios positivos con otros megativos. Estudiamos 4 pacientes, 3 hombres y una mujer, con un rango de edad de 33 a 55 años; el tiempo de evolución de la enfermedad osciló entre 1 y 14 años. Todos los pacientes tenían compromiso facial. Uno presentó lesiones múltiples y otro se acompañaba de lesiones extrafaciales. La inmunofluorescencia directa fue positiva en dos casos, hallando depósitos granulares de IgA en zona de membrana basal. La IgG, IgM, IgE y complemento fueron negativos en los 4 casos. Las distintas características de las inmunoglobulinas más un factor ambiental (rayos ultravioletas) u otro, llevaría a la IgA de la circulación a los tejidos. Posteriormente lo haría la IgG en la respuesta secundaria(AU)

Immune response and Trypanosoma cruzi infection in Trypanosoma rangeli-immunized mice.

The capacity of Trypanosoma rangeli antigens to induce immune response in mice was analyzed and the course of the infection was studied in immunized animals challenged with virulent forms of T. cruzi. BALB/c mice were immunized with supernatant of disrupted epimastigotes of T. rangeli and with epimastigotes (EPI) of T. rangeli fixed with glutaraldehyde. Both of the antigens were emulsified with incomplete Freund's adjuvant (IFrAdj). All of the animals received T. cruzi Tulahuen antigens in the footpad and the skin reactivity was later studied. The mice that received EPI with or without IFrAdj showed significantly higher skin reactivity than controls, both in Arthus (3 hr) and delayed type hypersensitivity (24 hr) reactions. Furthermore, the mice immunized with T. rangeli developed antibodies against T. cruzi detectable through hemagglutination and immunofluorescence tests. When the animals were challenged with trypomastigotes of T. cruzi, only the groups immunized with EPI-IFrAdj had significantly lower parasitemias and greater survival against infection than controls. These results suggest that T. rangeli can induce humoral and cellular immune response against T. cruzi and attenuate the acute period of the infection produced by this parasite. This is the first time that partial resistance to T. cruzi in T. rangeli-immunized mice is reported. These findings may provide a useful tool for future studies directed at the immunoprevention of Chagas' disease.

Suppression of active Arthus reaction by colchicine

An effect of colchicine on the active Arthus reaction in rabbits was investigated in vivo with simultaneous evaluation of in vitro chemotactic activity of polymorphonuclear leukocytes. Arthus reactions were induced by intracutaneous injection of ovalbumin into rabbits preimmunized with ovalbumin. Colchicine, 1 mg/kg or 2 mg/kg, injected intraperitoneally one hour prior to the induction of the Arthus reaction, suppressed erythema and induration at 12 h, when histology showed decreased numbers of C3, suggestive of the presence of immune complexes, persisted to 24 h. In vitro chemotaxis of polymorphonuclear leukocytes using Boyden chamber techniques revealed suppression of the activity in the colchicine-treated animals at 6 and 12 h. These findings suggest that colchicine inhibits vascular injury by interfering with directional chemotaxis of polymorphonuclear leukocytes to the lesional sites.

Sensitization to Schistosoma mansoni antigen in uninfected children born to infected mothers.

Sensitization to Schistosoma mansoni antigen in uninfected children born to infected or uninfected mothers was studied by intradermal reaction. Immediate skin reaction, Arthus phenomenon, and delayed skin responses were noted. The skin response at 24 hr was positive in 48.1% of the uninfected children born to infected mothers, and in only 7.5% of uninfected (control) children born to uninfected mothers. Areas of skin reactions were also larger in the group born to infected mothers. Both of these differences were statistically significant. There were no significant variations according to age or sex. Only one immediate skin reaction was noted in each group, and Arthus phenomenon was never observed.