| dc.description.abstract | The South American weed Parthenium hysterophorus, which was accidentally introduced into India in 1956, has successfully colonized several parts of the country. Being an alien weed, its uninhibited growth is posing agricultural and health hazards. It has been reported to be responsible for several hundred cases of allergic contact dermatitis in Poona (India), where it made its initial appearance. Waste lands and pasture fields are covered with a lush growth of this weed, and domestic animals that occasionally graze on them are likely to suffer from allergic manifestations. In addition, the pollen of this weed may be a source of naso?bronchial allergy in humans. Since no information is available on the health hazards associated with P. hysterophorus apart from its role in causing contact dermatitis, a systematic study was carried out to assess the role of this weed in causing various types of allergy.
Cases of contact dermatitis due to exposure to P. hysterophorus were identified in Bangalore. Clinical studies were carried out on 300 persons who were engaged in the manual eradication of this weed. It was observed that 56% of the weed pullers were sensitized by the weed, as indicated by positive patch test reactions. However, only 4% of them developed clinical symptoms of dermatitis. Patients suffering from Parthenium dermatitis were found to be sensitive to parthenin, the major sesquiterpene lactone of this plant, but not to its diastereoisomer, hymenin.
Since cattle and buffaloes were found to graze on this weed, studies were carried out to elucidate the role of Parthenium in causing Type IV hypersensitive reactions in domestic animals under laboratory conditions. It was found that buffalo bull calves, when fed with the fresh aerial parts of Parthenium, developed dermatitis. Intracorneal tests conducted on Parthenium?fed buffalo bull calves gave a positive reaction to parthenin but not to hymenin, suggesting that the dermatitis induced in these animals was a Type IV hypersensitive reaction mediated by sensitized lymphocytes.
An increase in the incidence of naso?bronchial allergy in Bangalore was noticed in recent years. In view of the possibility of Parthenium pollen being one of the causative agents of Type I hypersensitive reactions, an aerobiological survey was conducted for one year. These studies indicated that Parthenium pollen was wind?borne in significant amounts, either as individual pollen grains or in the form of clumps.
Mouse was chosen as the animal model system for the induction of reaginic (IgE) antibodies, since the pattern of IgE antibody production shows similarities with that observed in atopic humans. Persistent and boosterable IgE antibodies were induced to crude aqueous extracts of Parthenium pollen in three strains of mice, namely Swiss, C57Bl/Cri (low responders), and C3H/Cri (high responders). IgE antibodies were evaluated by passive cutaneous anaphylaxis (PCA) reaction. Treatment of low?responder mice with cyclophosphamide three days prior to the primary immunization resulted in enhanced IgE antibody production, thus converting low?responder mice to high responders.
The allergenic component(s) responsible for the induction of IgE antibodies in mice were isolated from the crude aqueous extracts of Parthenium pollen by DEAE?cellulose chromatography, Sephadex G?100 gel filtration, and polyacrylamide gel electrophoresis. Four proteins designated as I, II, III, and IV thus obtained were found to be homogeneous on polyacrylamide disc gel electrophoresis. The molecular weights of these proteins were found to be in the range of 32,000 to 58,000 daltons. The degree of allergenicity of these proteins, as evaluated by PCA reaction, was in the order: Protein IV > Protein II > Protein III > Protein I. Protein IV, the major allergen, was an acidic glycoprotein. This protein was found to be susceptible to heating, periodate oxidation, and digestion with chymotrypsin. Treatment with protein denaturants or sulphydryl reagents also resulted in a loss of allergenicity. The protein was, however, stable to digestion with trypsin.
Intracutaneous and prick tests were conducted on patients suffering from allergic rhinitis or bronchial asthma to assess the role of Parthenium pollen in causing Type I allergic reactions in humans. Total and allergen?specific IgE antibodies were determined in the sera of these patients by paper radioimmunosorbent test (PRIST) and paper radioallergosorbent test (PRAST), respectively. Allergen?specific IgE antibodies were present in the sera of those rhinitis patients who gave a positive intracutaneous or prick test reaction. Although patients suffering from bronchial asthma had elevated total serum IgE levels and gave positive skin reactions, their sera did not contain any allergen?specific IgE antibodies.
Sera of those rhinitis patients which showed a high percentage of binding to the crude extracts contained varying amounts of IgE antibodies specific to the purified pollen proteins. The relative binding capacity of the individual proteins was in the order: Protein IV > Protein I > Protein II > Protein III, as determined by PRAST. Comparison of the degree of allergenicity of these proteins in humans and in mice indicated that Protein IV was the major allergen in both systems. Protein I was, however, found to be more allergenic to humans than to mice. The allergenicity of Proteins II and III was in the same order in both systems. | |
