Impaired neutrophil and monocyte chemotaxis in chronic and aggressive periodontitis and effects of periodontal therapy.

Background and Objectives: Depressed chemotactic activity of polymorphoneutrophil (PMN) and monocyte (MN) appears to be one of the significant risk factors in the development of periodontal disease. Although bacteria are the primary etiologic factor in periodontal disease, the patient's host response is a determinant of disease susceptibility. Depressed chemotaxis of PMN and MN could lead to periodontal destruction by altering the host response i.e. impairment of the normal host response in neutralizing infection and alterations that result in destruction of the surrounding periodontal tissues. Materials and Methods: Thirty patients (10 healthy subjects, 10 chronic periodontitis, and 10 with aggressive periodontitis) participated in this study. Clinical parameters like plaque index, gingival index, probing pocket depth, and radiographic assessment were done. The peripheral blood PMNs and MNs were isolated from the patient and the chemotactic response was studied. Statistical analysis was performed using post-hoc Newman-Keul range test. Results: PMN and MN chemotaxis was found to be statistically significant (P<0.05) at baseline and three months after periodontal therapy in chronic and aggressive periodontitis group compared to healthy subjects. However on comparison between chronic and aggressive periodontitis group statistical significance was not found (P>0.05).Comparision between chronic periodontitis, aggressive periodontitis with healthy subjects, PMN and MN chemotaxis showed statistical significance (P<0.05) at baseline and three months after periodontal therapy, Whereas statistically there was no difference when chronic periodontitis was compared with aggressive periodontitis Interpretation and Conclusion: Depressed chemotaxis of PMN and MN results in increased periodontal destruction. In this study, depressed PMN and MN chemotaxis is seen in both aggressive periodontitis group and chronic periodontitis group and the response was altered although to a lesser degree after periodontal therapy in both groups indicating that effect of treatment does exist.

CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis

The comprehension of the pathogenesis of Trypanosoma cruzi-elicited myocarditis is crucial to delineate new therapeutic strategies aiming to ameliorate the inflammation that leads to heart dysfunction, without hampering parasite control. The augmented expression of CCL5/RANTES and CCL3/MIP-1alpha, and their receptor CCR5, in the heart of T. cruzi-infected mice suggests a role for CC-chemokines and their receptors in the pathogenesis of T. cruzi-elicited myocarditis. Herein, we discuss our recent results using a CC-chemokine receptor inhibitor (Met-RANTES), showing the participation of CC-chemokines in T. cruzi infection and unraveling CC-chemokine receptors as an attractive therapeutic target for further evaluation in Chagas disease.

Distribution of CD8 and CD20 lymphocytes in chronic periapical inflammatory lesions

O objetivo deste estudo foi o de investigar a distribuição de linfócitos CD8+ e CD20+ em lesões inflamatórias periapicais. Para tanto foram estudados 90 casos entre abscessos crônicos, cistos abscedados e cistos inflamatórios. A tecnica de imunohistoquímica pelo método da estreptavidina-biotina foi utilizada para identificar linfócitos T citotóxico/supressor (CD8) e linfócito B (CD20). Dentre os resultados encontrados notou-se uma distribuição das células CD8+ da seguinte forma: 1) difusa na capsula fibrosa dos abscessos crônicos (58,8 por cento) e ausente nos cistos abscedados (64,1 por cento) e cistos inflamatórios (70,6 por cento); 2) zona infiltrativa: difusa nos cistos abscedados (100 por cento) e cistos inflamatórios (82,4 por cento); 3) zona subepitelial: ausente nos cistos inflamatórios (53,0 por cento) e difusa nos cistos abscedados (56,4 por cento); 4) zona de supuração: difusa nos abscessos crônicos (100 por cento) e cistos abscedados (97,5 por cento). As células CD20+ apresentavam a seguinte distribuição: 1) cápsula fibrosa: ausente nos cistos inflamatórios (100 por cento), cistos abscedados (94,8 por cento) e abscessos crônicos (88,3 por cento); 2) zona infiltrativa: difusa nos cistos abscedados (100 por cento) e cistos inflamatórios (53 por cento); 3) zona subepitelial: ausente nos cistos inflamatórios (58,8 por cento) e focal nos cistos abscedados (46,2 por cento); 4) zona de supuração: difusa nos cistos abscedados (100 por cento) e abscessos crônicos (100 por cento). Em conclusão é possível afirmar que a distribuição linfocitária é predominantemente difusa para ambos os tipos de linfócitos.

Efecto de la cocaína y las catecolaminas sobre la quimiotaxis y la quimioluminiscencia de neutrófilos humanos in vitro

El objetivo fue determinar el efecto de la cocaína sola y mezclada con catecolaminas sobre la quimiotaxis y la explosión metabólica de los neutrófilos humanos y evaluar si la cocaína se une a estas células. La quimiotaxis se realizó en un gel de agarosa utilizando el péptido quimiotáctico FMLP. La explosión respiratoria se determino mediante la cuantificación de fotones (quimioluminiscencia) emitidos por las celulas activadas con PMA. Para cada prueba, las celulas se expusieron a concentraciones de cocaína de 1 a 1000ug/m y de catecolaminas 0.001 y 0.001 ug/mL y luego a la mezcla de 1000 ug/mL de cocaina con 0.001 ug/mL de catecolamina. La union de la cocaina a las celulas se evaluó mediante un ensayo de competición, con cocaína tritiada 10 nM y cocaína no radioactiva 500 uM. Los resultados no mostraron efecto de la cocaína quimiotaxis, pero sí aumento estadisticamente significativo (p=0.004), de la quimioluminiscencia de los neutrófilos tratados con 1000ug/mL de cocaína. Los valores de quimioluminiscencia sin cocaína fueron 1.2 x 10 a la 6 ñ 10 a la 4 cuentas por minuto (cpm) y con cocaina 1.7 x 10 a la 6 ñ1 x 10 a la 5 cpm. Las catecolaminas no modificaron los resultados obtenidos con la cocaina sola. La union de la cocaína tritiada a los neutrofilos tuvo un valor de 3.893 ñ 343 cpm, que disminuyó significativamente a 301 ñ 124 cpm en el ensayo de competición (p=0.008). Se demostró un incremento en la actividad metabólica de los neutrofilos inducido por cocaína, al parecer por su union a estas celulas. Estos resultados no son extrapolables a la clínica; sin embargo, el aumento de quimioluminiscencia debe ser tenido en cuenta, puesto que la exposición recurrente a la cocaína podría eventualmente conducir al mismo efecto

Evaluation of cell mediated immunity in healthy contacts of leprosy.

The cell mediated immunity (CMI) was studied in 50 healthy contacts of leprosy patients and 50 age & sex matched non-contact controls by lepromin test and leucocyte migration inhibition (LMI) test using phytohaemagglutinin (PHA) and lepromin and its association with other risk factors in contacts was assessed. The lepromin positivity correlated well with LMI results. There was no difference in CMI in I, II and III degree of contacts. Amongst direct contacts lepromin test was positive in 67 per cent as compared to 92 per cent in indirect contacts while in LMIT migration index (MI) was significantly increased (0.66 +/- 0.20) in direct contacts. MI was also significantly increased (0.73 +/- 0.20) contacts of less than two years duration which decreased to 0.51 +/- 0.18 in contacts of more than five years duration. Lepromin positivity also increased from 60 per cent to 100 per cent in these contacts. The specific CMI was significantly suppressed in contacts of LL patients (MI:0.74 +/- 0.21) and BL patients (MI: 0.61 +/- 0.01) as compared to healthy controls. B.C.G. vaccinated individuals showed better CMI response. The findings in the study showed specific unresponsiveness to lepromin in LMI in leprosy contacts of less than two years duration, direct contacts, contacts of lepromatous spectrum of index patients and contacts not vaccinated with B.C.G. emphasizing that CMI status is an important parameter in identifying the contact population at the greater risk of acquiring leprosy.

In vivo leucocyte chemotaxis in experimental mice Schistosoma mansoni infection

A quimiotaxia de leucocitos "in vivo" foi avaliada em camundongos da linhagem C57B1/10 e estudada 10, 30, 50 e 60 dias apos a infeccao por Schistosoma mansoni. A proteina A foi utilizada como quimiotatico e injetada no tecido conjuntivo no dorso dos camundongos dos grupos experimentais e controle. Nos grupos experimentais foi observado uma diminuicao na resposta dos leucocitos polimorfonucleares (PMN) em comparacao com o grupo controle (p<0.05). Os camundongos estudados 10 dias apos a infeccao, mostraram uma diminuicao na resposta quimiotatica de leucocitos PMN, comparando com o grupo controle (p<0.05) e este dado tornou-se mais evidente nos grupos experimentais estudados 30 e 50 dias apos a infeccao....