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Med J Aust. 2002 Sep 16;177 Suppl:S47-9.
The immunobiology of early asthma.

Anderson GP.

Department of Medicine, University of Melbourne, Parkville, VIC. gpnimelb.edu.au

What do we know? CD4+ T cells are strongly implicated in asthma pathogenesis. The "T(H)2 hypothesis" postulates two patterns of cytokine secretion by stimulated CD4+ T cells: a "T(H)1" response and a "T(H)2" response. T(H)2-type cytokines (interleukins IL-4, IL-5, IL-9, IL-13) regulate eosinophilia, mast cell growth, IgE and mucus production and have been proposed as key regulatory factors in asthma. T(H)1-type cytokines include interferon-gamma, IL-2, IL-12, IL-18, and tumour necrosis factor beta.T(H)2 responses are reciprocally inhibited by T(H)1 responses in animal models, but this may not be so in asthma in humans. In humans, T(H)1- and T(H)2-type cytokines are often coexpressed in early asthma. What do we need to know? Is cross-regulation between T(H)1 and T(H)2 immune biases truly lost in in early asthma? Can induction of T(H)1-type responses actually protect against asthma, as predicted by the "hygiene hypothesis"? If so, how might this induction be achieved safely in infants? Can the in-utero environment be subtly manipulated to minimise asthma risk? Does early childhood treatment with current anti-asthma drugs lead to long-term immune changes?

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225257&dopt=Abstract

Med J Aust. 2002 Sep 16;177 Suppl:S50-1.
Respiratory infections and asthma.

Isaacs D, Joshi P.

Department of Immunology and Infectious Diseases, The Children's Hospital at Westmead, University of Sydney, NSW. davidhw.edu.au

What we know: Respiratory viral infections caused by rhinoviruses, coronaviruses, influenza, parainfluenza and respiratory syncytial viruses (RSVs) are important triggers of asthma attacks. Mycoplasma and Chlamydia infections can also provoke asthma attacks, although less commonly. RSV infections probably do not cause asthma, but are potent triggers of wheezing, with the result that RSV infection often reveals underlying asthma in children. RSV infection does not cause atopy. Bacterial respiratory infections in infancy appear to protect against later atopy. What we need to know: Does RSV infection in infancy alter a child's T(H)1/T(H)2 responses to later infections with other respiratory pathogens? What are the mechanisms (immunological or mechanical) by which respiratory pathogens cause wheezing? What is the role of respiratory infections in exacerbations of asthma? Can epidemiology shed light on this? Do viruses such as RSV cause asthma or uncover underlying asthma? Do children respond differently to RSV than to other viruses? Does atopy affect those responses? Do bacterial respiratory infections truly protect against future atopy?

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225258&dopt=Abstract

Med J Aust. 2002 Sep 16;177 Suppl:S66-9.
Therapeutic prospects for early asthma.

Anderson GP.

Department of Medicine, University of Melbourne, Parkville, VIC. gpnimelb.edu.au

What we know: There is strong evidence that T cells contribute to asthma pathogenesis. Immune-modulating drugs that dampen, turn off or redirect T cells, and adjuvants that trigger T(H)1 immune responses, are potential therapies for preventing asthma. Current T cell immune suppressors are too toxic to use in very young children with asthma. Immune-modulation research is identifying pathways that might lead to preventive therapy for asthma. Inhibitors of T cell cytokines do not reduce asthma in adults. What we need to know: Is immune deviation from a T(H)2-type response towards a T(H)1-type response a sound strategy given that mixed T(H)1/T(H)2 responses are already known to occur in asthma? What, specifically, triggers the development of armed effector lymphocytes that are thought to cause tissue damage in asthma? Are the changes in lung structure that are observed in chronic asthma really dependent on T cell mechanisms? Can abnormal lung structure be improved or normalised? Would any of these strategies be safer and more effective than current therapies?

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225265&dopt=Abstract

Acta Neurol Scand. 2002 Oct;106(4):236-9.
Visual recovery in a man with the rare combination of mtDNA 11778 LHON mutation and a MS-like disease after mitoxantrone therapy.

Buhmann C, Gbadamosi J, Heesen C.

Department of Neurology, University Hospital Eppendorf, Hamburg, Germany. buhmanke.uni-hamburg.de

We describe a young man with prognostic unfavourable homoplasmatic mitochondrial DNA(mt DNA) 11778 Leber's hereditary optic neuropathy (LHON) point mutation and confirmed multiple sclerosis (MS). This combination of LHON and MS-like disease is rare in both sexes, and in men has been described in only a few case reports. In a 4-year follow-up during immunosuppressive therapy with mitoxantrone, we found a remarkable time delayed visual recovery 12 months after acute onset of rapid sequential bilateral subtotal visual loss followed by episodes of isolated acute demyelinative optic neuropathy. Visual recovery to such extent after this latency is uncommon in both mtDNA 11778 LHON mutation and optic neuritis (ON) in MS. Relapses in visual deterioration must be considered as extremely rare in LHON. This case might support the hypothesis of an immunological pathogenetic factor in combined LHON and MS, and possibly in LHON alone. We suggest a search for the LHON mutation in MS patients with predominant visual impairment, independent of patients' gender.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225323&dopt=Abstract

Immunology. 2002 Sep;107(1):145-51.
Expression and regulation of the pattern recognition receptors Toll-like receptor-2 and Toll-like receptor-4 in the human placenta.

Holmlund U, Cebers G, Dahlfors AR, Sandstedt B, Bremme K, Ekstrom ES, Scheynius A.

Department of Medicine, Karolinska Hospital and Insitutet, Stockholm, Sweden. ulrika.holmluns.se

The placenta constitutes a physical and immunological barrier against invading infectious agents and has been suggested to be a pregnancy-specific component of the innate immune system. The aim of this study was to investigate the presence and regulation of Toll-like receptors-2 and -4 (TLR2 and TLR4) in the human placenta, because these receptors are believed to be important for immune responses against pathogens. Twenty-eight placentas from normal term pregnancies were analysed with immunohistochemistry, which showed a strong immunoreactivity for TLR2 and TLR4 in the villous and the intermediate trophoblasts. The regulation of TLR2 and TLR4 by microbial stimulus was assessed by incubating explants of term chorionic villi with zymosan or lipopolysaccharide (LPS) and analysed with real-time reverse transcriptase-polymerase chain reaction. Stimulation with zymosan and LPS readily induced interleukin (IL)-6 and IL-8 cytokine production in the placenta cultures, whereas TLR2 and TLR4 mRNA and protein expression remained at the same high level as in unstimulated explants. These data suggests a novel mechanism for the fetoplacental unit to interact with micro-organisms.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225373&dopt=Abstract

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