Few microorganisms are as versatile as Escherichia coli. An important member of the normal intestinal microflora of humans and other mammals, E. coli has also been widely exploited as a cloning host in recombinant DNA technology. But E. coli is more than just a laboratory workhorse or harmless intestinal inhabitant; it can also be a highly versatile, and frequently deadly, pathogen. Several different E. coli strains cause diverse intestinal and extraintestinal diseases by means of virulence factors that affect a wide range of cellular processes.

Pathogenic Escherichia coli

Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the membranes lining the nose. It is a global health problem that causes major illness and disability worldwide. Over 600 million patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work and its economic impact is substantial. Risk factors for allergic rhinitis are well identified. Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations.

In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) WHO workshop, the expert panel proposed a new classification for allergic rhinitis which was subdivided into 'intermittent' or 'persistent' disease.

This classification is now validated. The diagnosis of allergic rhinitis is often quite easy, but in some cases it may cause problems and many patients are still under-diagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work.

The management of allergic rhinitis is well established and the ARIA expert panel based its recommendations on evidence using an extensive review of the literature available up to December 1999. The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. A large number of papers have been published since 2000 and are extensively reviewed in the 2008 Update using the same evidence-based system. Recommendations for the management of allergic rhinitis are similar in both the ARIA workshop report and the 2008 Update. In the future, the GRADE approach will be used, but is not yet available.

Another important aspect of the ARIA guidelines was to consider co-morbidities. Both allergic rhinitis and asthma are systemic inflammatory conditions and often co-exist in the same patients. In the 2008 Update, these links have been confirmed.

The ARIA document is not intended to be a standard-of-care document for individual countries. It is provided as a basis for physicians, health care professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients.

/pdf/allergic-rhinitis-and-its-impact-on-asthma-aria-2008-update-13eqfzaw4u.pdf

Allergic rhinitis and its impact on asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen)

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(07)61692-4.pdf

Maternal and child undernutrition: consequences for adult health and human capital.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(05)71142-9.pdf

Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.

The hygiene hypothesis postulates that an environment with a high incidence of infectious diseases protects against allergic and autoimmune diseases, whereas hygienic surroundings increase the incidence of these disorders This review examines the evidence in support of the hygiene hypothesis and offers a number of mechanisms that could explain the relation between sanitary conditions and susceptibility to allergic and autoimmune diseases

https://www.nejm.org/doi/pdf/10.1056/NEJMra020100

The Effect of Infections on Susceptibility to Autoimmune and Allergic Diseases

Examination of 77 strains of Escherichia coli from the cerebrospinal fluid of neonates with meningitis revealed 65 (84 per cent) with the capsular (K1) polysaccharide The Esch coli K1 ca

https://www.nejm.org/doi/pdf/10.1056/NEJM197405302902202?listPDF=true

Escherichia coli K1 capsular polysaccharide associated with neonatal meningitis.

Objectives The reader of this review will learn about the mechanisms through which breastfeeding protects against infections during and most likely after lactation, as well as possibly against certain immunologic diseases, including allergy. Data sources I have followed the literature in the area closely for the last 30 to 40 years and have made repeated literature searches through MEDLINE, most recently in 1998. Textbooks and peer-reviewed journals have been sought for, as well as books representing meeting reports in English, French, German, and Spanish. Results Human milk protects against infections in the breastfed offspring mainly via the secretory IgA antibodies, but also most likely via several other factors like the bactericidal lactoferrin. It is striking that the defense factors of human milk function without causing inflammation, some components are even directly antiinflammatory. Protection against infections has been well evidenced during lactation against, eg, acute and prolonged diarrhea, respiratory tract infections, otitis media, urinary tract infection, neonatal septicemia, and necrotizing enterocolitis. There is also interesting evidence for an enhanced protection remaining for years after lactation against diarrhea, respiratory tract infections, otitis media, Haemophilus influenzae type b infections, and wheezing illness. In several instances the protection seems to improve with the duration of breastfeeding. Some, but not all studies have shown better vaccine responses among breastfed than non-breastfed infants. A few factors in milk like anti-antibodies (anti-idiotypic antibodies) and T and B lymphocytes have in some experimental models been able to transfer priming of the breastfed offspring. This together with transfer of numerous cytokines and growth factors via milk may add to an active stimulation of the infant's immune system. Consequently, the infant might respond better to both infections and vaccines. Such an enhanced function could also explain why breastfeeding may protect against immunologic diseases like celiac disease and possibly allergy. Suggestions of protection against autoimune diseases and tumors have also been published, but need confirmation. Conclusions Breastfeeding may, in addition to the well-known passive protection against infections during lactation, have a unique capacity to stimulate the immune system of the offspring possibly with several long-term positive effects

Breastfeeding provides passive and likely long-lasting active immunity

IT has been suggested that feeding infants with human milk reduces the incidence of gastrointestinal infections1. Although macrophages, lymphocytes and antibodies in the milk are probably important in this protection2,3, the mechanism for the development of specific immunity to enteric pathogens is not known. Human colostral cells synthesise IgA (ref. 4), and we have used the haemolysis-in-gel technique to demonstrate that human colostrum contains numerous cells which produce IgA antibodies against the O antigens of commonly encountered Escherichia coli bacteria5. This suggested that the sensitised lymphocytes had either undergone antigen-induced clonal proliferation within the mammary gland or had homed to that organ from another site after becoming sensitised. Because of reports that gastrointestinal immunisation of germ-free mice led to local6 and systemic7 production of IgA antibodies, and that cells from Peyer's patches effectively repopulate the ileum of lethally-irradiated rabbits with IgA-producing cells8, we have examined the effect of gastrointestinal immunisation on the development of antibody-producing cells in colostrum of humans. We found that oral administration of a non-pathogenic strain of E. coli led to the rapid appearance of colostral cells producing antibodies against the O antigen of the organism.

Antibody-forming cells in human colostrum after oral immunisation.

Lactoferrin down-regulates the LPS-induced cytokine production in monocytic cells via NF-κB

Human milk inhibited the attachment of Streptococcus pneumoniae and Haemophilus influenzae to human pharyngeal or buccal epithelial cells. Infant formulas and cow and buffalo milk showed a lower inhibitory activity against pneumococci and enhanced the adhesion of H. influenzae. The antiadhesive effect against S. pneumoniae was found in both the high- and the low-molecular-weight fractions of milk. The inhibitory activity in the high-molecular-weight fraction was independent of specific antibody content; it was present after immunoadsorption and in the milk from IgA-deficient women. The inhibitory activity in the low-molecular-weight fraction was in part explained by the content of oligosaccharides corresponding to the carbohydrate moieties of the neolactoseries of glycolipids, which have previously been shown to act as receptors for attaching pneumococci. The antiadhesive activity against H. influenzae was restricted to the high-molecular-weight fraction of the milk and was unaffected by immunoadsorption. Milk may protect against otitis by reducing colonization.

Lars Å. Hanson

Papers

Escherichia coli K1 capsular polysaccharide associated with neonatal meningitis.

Breastfeeding provides passive and likely long-lasting active immunity

Antibody-forming cells in human colostrum after oral immunisation.

Lactoferrin down-regulates the LPS-induced cytokine production in monocytic cells via NF-κB

Inhibition of Attachment of Streptococcus pneumoniae and Haemophilus influenzae by Human Milk and Receptor Oligosaccharides