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Levels of interleukin-2 (IL-2) in serum obtained from human immunodeficiency virus (HIV)- infected children at health maintenance visits were measured to characterize endogenous IL-2 responses and to examine the association between these responses and progression of immunosuppression. IL-2 was detectable (level >8.7 pg/mL) in the serum of 28 of 45 HIV-infected children; 42% (19 of 45) had serum IL-2 levels of >39 pg/mL. Children without evidence of immunosuppression (Centers for Disease Control and Prevention Pediatric HIV Classification Immunologic Category 1, n = 15) and children with severe immunosuppression (immunologic category 3, n = 20) had statistically significant lower serum IL-2 levels (mean ± [SD], 134.4 ± 227.3 pg/mL and 18.2 ± 30.3 pg/mL, respectively) than those with moderate immunosuppression (mean ± [SD], 450.5 ± 311.8 pg/ml; immunologic category 2, n = 10) (P < .05, Wilcoxon rank sum test). In those children in whom immunosuppression was evident, decreasing serum IL-2 levels correlated with depletion of CD4+ lymphocytes (r = 0.74), whereas there was an inverse correlation between serum IL-2 levels and CD4+ lymphocyte counts (r=−0.47) in children with no or moderate immunosuppression.

To guide the decision-making for the case definition and guidelines, a literature search was performed by a Cochrane Collaboration professional search person for Guillain-Barré syndrome and other peripheral neuropathies in the context of immunization (MEDLINE 1976-2006; search terms included among others \"Guillain-Barré syndrome\", \"acute inflammatory demyelinating polyradiculoneuropathy\", \"peripheral neuropathy\", \"peripheral demyelination\", \"vaccine\", and \"immunization\"). First described by French neurologists Guillain, Barré, and Stohl in 1916, understanding of the disorder has increased tremendously in the past 2 decades [5]. 0 Healthy 1 Minor symptoms or signs of neuropathy but capable of manual work/capable of running 2 Able to walk without support of a stick (5m across an open space) but incapable of manual work/running 3 Able to walk with a stick, appliance, or support (5m across an open space) 4 Confined to bed or chair bound 5 Requiring assisted ventilation (for any part of the day or night) 6 Death

There is marked activation of the endothelium and immune system in Kawasaki disease. Anticardiolipin antibodies (aCL) can cause activation of the endothelium. We measured aCL levels in acute Kawasaki disease patients and compared them to other febrile patients to see whether their aCL responses were different. Twenty-one patients with acute Kawasaki disease and 16 patients with an acute febrile illness were recruited. The aCL levels were measured in the sera of febrile patients and in Kawasaki disease patients prior to immunoglobulin therapy. There was no significant difference between the IgG aCL levels (p = 0.87) between the Kawasaki disease and febrile patients. However, the IgM (p = 0.01) and IgA (p = 0.03) aCL were significantly higher in patients with acute Kawasaki disease than in febrile children. Elevation of IgA aCL has been reported in association with other vasculitides and IgA-secreting plasma cells have been demonstrated in the vascular tissue in Kawasaki disease.

Current evidence supports the concept that oral administration of probiotic lactobacilli may be therapeutic in preventing antibiotic-associated diarrhea in children and in reestablishing normal flora in the gastrointestinal tract. Children with human immunodeficiency virus (HIV) infections may have episodes of diarrhea and frequently experience malabsorption associated with possible bacterial overgrowth; together these may interact to produce the growth abnormalities characteristic of this group. The overall objective of this investigation has been to determine whether oral administration of the probiotic Lactobacillus plantarum 299v could improve nutrient status and promote growth in children congenitally exposed to HIV. In addition, the possible beneficial effect of Lactobacillus plantarum 299v in modulating immune response was evaluated. In preliminary results described here, we report on the ability of Lactobacillus plantarum 299v to colonize children with HIV and to elicit specific systemic immune response after oral supplementation.

Intravenous immune gamma-globulin (IVIG) is used successfully in the treatment of Kawasaki disease, with dose-dependent rapid resolution of symptoms such as fever and irritability and a decrease in ESR, WBCs, and platelets. The mode of action of IVIG in reducing this inflammatory response is not clearly understood. Recently anticytokine antibodies in IVIG have been demonstrated. Serum levels of proinflammatory cytokines have been shown to be elevated in patients with Kawasaki disease. The cytokine interleukin-6 (IL-6) is involved in the de novo production of acute-phase proteins by hepatocytes and cause thrombocytosis and fever in response to tissue injury. Patients receiving parenteral recombinant human IL-6 have dose-dependently experienced fever, malaise, chills, and acute-phase reaction. With high IL-6 concentrations, central nervous system toxicity has also been reported and IL-6 has been thought to mediate endothelial damage. We evaluated the response of stimulated blood cells of 12 normal children to IVIG in the release of the cytokines IL-6, IL-8, TNF-alpha. and IL-6 receptor (sIL-6R). The levels of cytokines IL-6, IL-8, and TNF-alpha (but not sIL-6R) in peripheral blood induced by stimulation with LPS were markedly reduced (P < 0.008) within 3 hr when incubated with IVIG compared to without IVIG. Thus we demonstrated that cells of normal children respond to IVIG in vitro by reducing cytokines such as IL-8, TNF-alpha, and IL-6 without affecting the level of receptor sIL-6R during an acute inflammatory response. We also found significantly higher IL-6 levels in children with Kawasaki disease compared to children with blood culture-negative febrile illnesses. In five children with Kawasaki disease we measured serum IL-6 before and after IVIG and assessed the clinical response to IVIG therapy. Therapy with IVIG was followed by a rapid resolution of symptoms in Kawasaki disease, with a significant decrease in serum IL-6. The attenuation of proinflammatory cytokine responses, especially IL-6, following infusions of IVIG may play an integral role in the rapid resolution of symptoms and decrease in the acute-phase proteins in children with Kawasaki disease. Cells of normal children were found to respond to the IVIG in a manner similar to that of the Kawasaki children.

► We evaluate CNS pathology of 37 children receiving standard vaccine. ► Clinical features correlated well with pathologic features. ► Vaccines do not cause permanent/lethal CNS damage. Documentation of clinical-pathological features of 37 infants/children whose parents alleged a relationship between vaccination and death or permanent central nervous system (CNS) damage, and sought compensation through the National Vaccine Injury Compensation Program. Of the 5545 claims filed during the 10-year period (1990–1999), CNS tissue was available for evaluation by a pediatric neuropathologist in 37; 33 died and 4 had a biopsy or lobectomy. Most commonly implicated vaccines were DTP/DTaP, followed by MMR and IPV/OPV, but almost all of the vaccines currently given to infants/children were alleged to be responsible for the illness/death. No lesions were found in 5 of 37 (13.5%). The most frequent abnormality consisted of acute anoxic encephalopathy (14 of 37 – 37.8%), consequent to several different causes, such as positional asphyxia, cardio-respiratory arrest during status epilepticus, etc. The remaining children manifested other lesions, including inflammation (5 of 37 – 13.5%), vascular and developmental anomalies (4 each of 37 or 10.6%), cerebral edema and system degeneration (2 each of 37 or 5.4%), and one case of heavy metal exposure in a child living near an abandoned mine (2.2%). There was no obvious relationship between type of vaccine (or vaccines simultaneously administered) to time of onset of symptoms, nature of symptoms or the lesions found.

The hypothesis that probiotic administration protects the gut surface and could delay progression of Human Immunodeficiency Virus type1 (HIV-1) infection to the Acquired Immunodeficiency Syndrome (AIDS) was proposed in 1995. Over the last five years, new studies have clarified the significance of HIV-1 infection of the gut associated lymphoid tissue (GALT) for subsequent alterations in the microflora and breakdown of the gut mucosal barrier leading to pathogenesis and development of AIDS. Current studies show that loss of gut CD4+ Th17 cells, which differentiate in response to normal microflora, occurs early in HIV-1 disease. Microbial translocation and suppression of the T regulatory (Treg) cell response is associated with chronic immune activation and inflammation. Combinations of probiotic bacteria which upregulate Treg activation have shown promise in suppressing pro inflammatory immune response in models of autoimmunity including inflammatory bowel disease and provide a rationale for use of probiotics in HIV-1/AIDS. Disturbance of the microbiota early in HIV-1 infection leads to greater dominance of potential pathogens, reducing levels of bifidobacteria and lactobacillus species and increasing mucosal inflammation. The interaction of chronic or recurrent infections, and immune activation contributes to nutritional deficiencies that have lasting consequences especially in the HIV-1 infected child. While effective anti-retroviral therapy (ART) has enhanced survival, wasting is still an independent predictor of survival and a major presenting symptom. Congenital exposure to HIV-1 is a risk factor for growth delay in both infected and non-infected infants. Nutritional intervention after 6 months of age appears to be largely ineffective. A meta analysis of randomized, controlled clinical trials of infant formulae supplemented with Bifidobacterium lactis showed that weight gain was significantly greater in infants who received B. lactis compared to formula alone. Pilot studies have shown that probiotic bacteria given as a supplement have improved growth and protected against loss of CD4+ T cells. The recognition that normal bacterial flora prime neonatal immune response and that abnormal flora have a profound impact on metabolism has generated insight into potential mechanisms of gut dysfunction in many settings including HIV-1 infection. As discussed here, current and emerging studies support the concept that probiotic bacteria can provide specific benefit in HIV-1 infection. Probiotic bacteria have proven active against bacterial vaginosis in HIV-1 positive women and have enhanced growth in infants with congenital HIV-1 infection. Probiotic bacteria may stabilize CD4+ T cell numbers in HIV-1 infected children and are likely to have protective effects against inflammation and chronic immune activation of the gastrointestinal immune system.