Latin name: Ambrosia elatior (Synonym: Ambrosia artemisifolia)
Source material: Pollen
Family: Asteraceae (Compositae)
Common names: Common ragweed, Annual ragweed, Short ragweed, Roman wormwood, American wormwood
Synonyms: A. artemisifolia
Common (Short) ragweed is native to North America, but can also be found in Canada, Japan, Australia and Europe. It is a prime cause of allergy in the US, and now in Europe, in particular in the upper Rhône valley, the Balkan states and the Krasnodar district of the Russia.
Common (Short) ragweed is an erect summer annual herbaceous plant growing to 0.9 m. The leaves are soft, green and opposite or alternate. Each leaf is divided into narrow segments, which are in turn irregularly lobed. It closely resembles False ragweed. Short ragweed produces burs similar to those of Giant ragweed, but the former are considerably smaller (2 to 4 mm long).
Short (Common) ragweed flowers from August to October. It is wind-pollinated, releasing millions of pollen grains into the air. However, the presence of the pollen in honey indicates some insect pollination.
Male and female flowers are in separate heads on the same plant (a monoecious structure). The tiny, nodding, greenish staminate (male) flowers, usually drooping, are in slender racemes near the top of the plant, while the pistillate (female) flowers tend to cluster at the bases of the racemes.
The Ragweed pollination period extends from the beginning of August to mid-October with a peak from mid-August to the end of September. Ragweed pollen release begins at sunrise and continues during the morning, reaching its highest count around midday. Pollen release is maximal in sunny and dry weather, and when night temperature is above 10° C. The pollen of A. artemisiifolia is produced in enormous amounts compared to other grasses, and a single plant alone may produce millions of pollen grains. Since the pollen grains are small (18–22 µm), they are often transported long distances. Ragweed pollen is very allergenic, and very low concentrations such as 5–10 pollen by cubic meter of air are sufficient to trigger allergic reactions in sensitive patients (1).
Short Ragweed is found in woodland and waste places. It occurs on dry fields and pastures, along roadsides, and especially in disturbed soil sites. It can become a pernicious weed in cultivated soils.
The leaves of the plant are used in herbal medications. A tea made from the roots is used as a herbal remedy. The pollen is harvested commercially and manufactured into homeopathic preparations for the treatment of allergies to the plant.
Ragweed contains numerous allergens. Among these allergens, 22 are already well known and 6 are considered major. Several ragweed pollen allergens have been characterised at the molecular level. Amb a 1 is the most important allergen, since 95% of Ragweed-sensitive individuals react to the protein in skin tests and show high serum IgE antibody titers (1-4).
The following allergens have been characterised:
Amb a 1, a 38 kDa protein, a pectate lyase, also known as Antigen E, AgE, a24, a789 and previously as Amb a I, Amb e 1 (3,5-15).
Amb a 2, a 38 kDa protein, a pectate lyase, also known as Antigen K, AgK, and previously as Amb a II, Amb e 2 (3,7,10-11,14,16-17).
Amb a 3, a 9 kDa protein also known as Ra3, and previously as Amb a III, Amb e 3 (7,18-22).
Amb a 5, a 5 kDa protein, also known as Ra5, Ra5S, and previously as Amb a V, Amb e 5 (9,21,23-29).
Amb a 6, a 10 kDa protein, a lipid transfer protein, also known as Ra6 and previously as Amb a VI (2,7,21,30-33).
Amb a 7, a 12 kDa protein, also known as Ra7 (7,34.)
Amb a 8, a 14 kDa protein, a profilin (7,35-38).
Amb a 9, a 10kDa protein, a calcium-binding protein (7,36).
Amb a 10, a 10kDa protein, a calcium-binding protein (7,36,39-40).
Amb a Cystatin Prot Inhibitor (41).
Isoforms of Amb a 1 have been identified: Amb a 1.1, Amb a 1.2, Amb a 1.3, Amb a 1.3, and Amb a 1.4 (10).
Amb a 1 and Amb a 2 have been shown to display immunological cross-reactivity in ELISA studies (9).
With the use of a serum pool from patients sensitive to Short ragweed, the cross-reactivity of IgE antibodies to six Ragweeds was studied through the radioallergosorbent test. Extracts were analysed for their inhibitory activities, with solid-phase allergens prepared from all of the Ragweed pollens. Also, samples of serum were absorbed with the various solid-phase allergens and the reactivity of the remaining IgE antibodies was determined. Two patterns of reactivity were observed. Short, Giant, Western, and False ragweeds displayed comparable reactivity in both inhibition and absorption experiments. Slender and Southern ragweed were considerably less active, indicating that they lacked allergenic groupings possessed by the other species. These same patterns of cross-reactivity were found using Ragweed pollens from four commercial sources (42).
Further cross-reactivity among the various Ragweeds can be inferred due to the high cross-reactivity among various other members of the genus Ambrosia and of the family Asteraceae. For example, cross-reactivity among Chamomile tea extract, pollen of Matricaria chamomilla, Artemisia vulgaris (Mugwort), and Ambrosia trifida (Giant ragweed) was demonstrated by an ELISA-inhibition study (43). Further evidence confirming cross-reactivity among members of the Ragweed genus was obtained in a study using a fluorescent allergosorbent test, in which similar antigenic determinants were found among Short and Giant ragweed, Cocklebur, Lamb’s quarters, Rough pigweed, Marshelder, and Goldenrod. Cocklebur and Giant ragweed were highly potent in their ability to competitively bind to Short ragweed IgE. The other pollens demonstrated lower potency of cross-reacting antigens (44). Also, a water-insoluble material, extracted from Short ragweed and False ragweed pollen, contained at least five proteins. Two (RFA2 and RFB2) were isolated and shown to possess antigenicity as well as allergenicity. Immunodiffusion tests of RFB2, isolated from False ragweed and Short ragweed, showed immunological identity (45).
However and surprisingly, Common ragweed and Giant ragweed are not allergenically equivalent because of allergenic differences involving both the major allergens Amb a 1-2 and Amb t 1-2 (all members of the pectate lyase family) and some minor allergens (46). This is illustrated by the example from an area north of Milan (a zone widely invaded only by Short ragweed), where about 50% of patients treated with specific immunotherapy (SIT) with Giant ragweed who showed little or no clinical response to SIT, but showed an excellent outcome if they were shifted to SIT with Short ragweed. These authors suggested that in patients allergic to Ragweed, both diagnosis in vivo and immunotherapy should always be performed by using the ragweed species present in that specific geographic area (49).
Sensitisation to Amb a 1, a pectate lyase, results in cross-reactivity only with other pectate lysase containing plants where a high degree of homology occurs. Not all proteins in this family are allergens. The allergens in this family include: Amb a 1, Amb a 2, Cha o 1 (Japanese Cypress tree), Cup a 1 (Arizona Cypress tree), Cry j 1 (Japanese Cedar tree), Jun a 1 (Mountain Cedar tree) (47).
Furthermore, Mugwort, Ragweed, and Timothy grass pollen share IgE epitopes with Latex glycoprotein allergens. The presence of common epitopes might in part explain clinical symptoms on contact with Latex in patients allergic to pollen. In this study, any previously known panallergen was not detected (48).
An association between Ragweed pollinosis and hypersensitivity to Cucurbitaceae vegetables (e.g., Watermelon, Cantaloupe, Honeydew Melon, Zucchini, and Cucumber) and Banana has been reported. Up to now three allergens have been identified as candidates for causing this cross-reactivity: profilin, Bet v 1, and a 60-69 kd allergen (49). Further evidence for cross-reactivity between Cucurbitaceae and Ragweed was found in a study that reported that of the sera of 192 allergic patients, 63% contained anti-Ragweed IgE, and among these patients, 28% to 50% had sera containing IgE specific for any single gourd family member. The extracts of Watermelon and Ragweed inhibited each other in a dose-dependent manner (50).
Ragweed profilin can be expected to result in cross-reactivity between this plant and other plants containing profilin. This has been demonstrated between Ragweed and Persimmon (44). In a second study, 35 of 36 patients’ sera containing IgE to Ragweed profilin reacted with profilin from Latex, indicating structural homologies between profilin from Latex and Ragweed. Because profilin is also present in Banana extract, it is likely to be involved in cross-sensitivity between Banana and Latex (43).
In addition to profilin, Mugwort and Ragweed pollen contain a number of other cross-reactive allergens, among them the major Mugwort allergen Art v 1. These cross-reactive IgE antibodies could result in clinically significant allergic reactions (34). Evidence of further cross-reactivity between Mugwort and other members of the Asteraceae family (of which Ragweed is a member) consists in the high degree of in vivo cross-reactivity between Matricaria chamomilla (Camomile) and Mugwort (51).
Cross-reactivity between Sunflower and other Asteraceae pollens (Mugwort, Marguerite, Dandelion, Goldenrod, and Short ragweed) has also been demonstrated by RAST and immunoblotting inhibition experiments. Mugwort pollen exhibited the greatest degree of cross-reactivity with Sunflower pollen, whereas at the other end of the spectrum, Short ragweed showed fewer cross-reactive epitopes (52).
Celery cross-reacting to Ragweed has also been reported, but a panallergen was not identified in these studies (53-54).
Binding to IgE from Ginkgo pollen proteins (Ginkgo biloba L.) was shown to be almost completely inhibited by Oak, Ryegrass, Mugwort and Ragweed, but only partially by Japanese Hop and rBet v 2 (55). A panallergen may be indicated but was not isolated.
Sera from subjects allergic to White Cypress Pine, Italian cypress, Ryegrass or Birch pollen were shown to have IgE antibodies that reacted with pollens from these four species and from Cocksfoot, Couch grass, Lamb’s quarters, Wall pellitory, Olive, Plantain and Ragweed. The authors concluded that the presence of pollen-reactive IgE antibodies may not necessarily be a true reflection of sensitising pollen species (56).
The Japanese cypress tree pollen allergen, Cha o 1, has a 46 to 49% similarly to the major allergens of Short ragweed, Amb a 1 and Amb a 2 (57).
A panallergen has been identified in Birch pollen, Ragweed pollen, Timothy grass pollen, Celery, Carrot, Apple, Peanut, Paprika, Anise, Fennel, Coriander and Cumin. EAST inhibition and immunoblot inhibition demonstrated that cross-reactions between Mango fruits, Mugwort pollen, Birch pollen, Celery, and Carrot are based on allergens related to Bet v 1 and Art v 1, the major allergens of Birch and Mugwort pollen, respectively (58).
Pollen of Artemisia annua is considered to be one of the most important allergens in autumnal hay fever in China, just as Ragweed is in North America. Extracts of pollen-free Artemisia annua components were found to contain similar allergens to those of Ragweed pollen. In 52 subjects sensitive to Artemisia pollen, 92.3% were shown on skin prick testing to have allergen-specific IgE to this allergen, 100% gave positive responses in intradermal tests, 66.7% gave positive responses in intranasal challenges, and 59.3% gave positive responses in bronchial provocation tests (59).
Ragweed pollen appears to also be cross-reactive with pollen from Yellow dock (Rumex crispus). When monoclonal antibodies with different specificity were applied against the major allergenic components of Ragweed pollen, the monoclonal antibodies reacted with antigens of Yellow dock pollen. In a preliminary study, sera of 2 patients containing IgE antibodies to Ragweed pollen antigens also reacted to the 40K component of Yellow dock pollen. In allergen-specific IgE tests on 109 patients with bronchial asthma, 22 had a positive reaction to a crude extract of Ragweed pollen, and 18 also reacted to a crude extract of Yellow dock pollen (60).
Ragweed, and in particular Short ragweed (A. artemisiifolia), is clinically the most important source of seasonal aeroallergens, as it is responsible for both the majority of cases and the most severe cases of allergic rhinitis (61-66). Ragweed pollen also contributes significantly to exacerbation of asthma and allergic conjunctivitis. Ragweed pollen has also been implicated in eustachian tube dysfunction in patients with allergic rhinitis (67) and contact dermatitis (68).
The efficacy of Ragweed pollen in exacerbating allergic symptoms may be due to the Ragweed pollen endopeptidase, which may be involved in the inactivation of regulatory neuropeptides during pollen-initiated allergic reactions (69). Studies have also shown that complement activation induced by the allergen may enhance the clinical symptoms of Ragweed allergy (70-71).
A genetic susceptibility to Ragweed allergens has been suggested based on HLA studies; Amb a V, Amb t V and Amb p V from Short ragweed, Giant ragweed and Western ragweed respectively are strongly associated with HLA-DR2 and Dw2 (DR2.2) in allergic Caucasoid individuals (72).
The measurement of specific IgE has been shown to be an accurate and useful diagnostic tool in the evaluation of sensitisation to Ragweed pollen (73-76).
Aerobiological and clinical studies from various cities in the USA have documented the importance of Ragweed pollen as an aeroallergen (77). Ragweed has been shown to contribute to symptoms in studies in Washington, DC (78), Tucson, Arizona (79), and Tulsa, Oklahoma (80).
The prevalence of Ragweed pollinosis in central Pennsylvania was shown to be significantly greater in the rural subjects than in inner-city ones (81). In Boston women, socio-economic differences in sensitisation to Ragweed differed between the highest and lowest poverty areas (49% vs. 23%) (82). Ragweed was shown to be a major aeroallergen in the Tampa Bay area, Florida (83).
In Chicago residents with asthma, Ragweed sensitivity occurred in 45%, more than those sensitised to pollen from all other weeds (42%) (84).
In a collaborative study on Parthenium hysterophorus pollen compared to an extract of Western Ragweed, a study contributed to by 22 physicians from 18 Gulf Coast cities, 65.6% overall of the sera tested were positive for one or both of the pollen extracts examined. Thirty-five percent of the sera were sensitive to Parthenium hysterophorus and 57.6% were sensitive to Ragweed. Thirty percent of the sera were positive to Western Ragweed only, 8% were positive to Parthenium hysterophorus only, and 27.9% were positive to both extracts (85-86). These studies support the findings of another study that examined cross-reactivity of allergens from the pollen of Parthenium hysterophorus (American Feverfew) and Ragweed in 2 groups of patients with different geographic distributions. Parthenium-sensitive Indian patients, who were never exposed to Ragweed, had positive skin reactions to Ragweed pollen extracts. A significant correlation in the RAST scores of Parthenium- and Ragweed-specific IgE was observed with the sera of Parthenium- and Ragweed-sensitive Indian and US patients, respectively. RAST inhibition experiments demonstrated that in the sera of Ragweed-sensitive patients the binding of IgE antibodies to Short and Giant ragweed allergens could be inhibited by up to 94% by Parthenium pollen extracts. Inhibition up to 82% was obtained when the sera of Parthenium rhinitis patients were incubated with Ragweed allergen extracts. The high degree of cross-reactivity between Parthenium and Ragweed pollen allergens suggests that individuals sensitised to Parthenium may develop type-I hypersensitivity reactions to Ragweed even though they never had contact with Ragweed, and vice versa (87).
In Canada, Ragweed pollinosis studies have been conducted in Quebec. Of 3,371 subjects with a clinical diagnosis of symptomatic asthma or rhinitis, Ragweed sensitisation was documented in 44.9% (88). Ragweed pollen was shown to be the principal allergen causing allergic rhinitis (89).
In Europe, the severity of Ragweed pollinosis varies according to geographical region. Expansion of the Ragweed genus is occurring across Europe, in particular in France, northern Italy, Austria, and Hungary (90).
Ragweed pollinosis has become a rapidly emerging problem in Italy (64). In 21 centres across Italy, in 2,934 consecutive outpatients with respiratory pathology of suspected allergic origin, 28.2% were positive to at least one “emerging” pollen: Birch, Hazelnut, Alder, Hornbeam, Cypress, or Ragweed. Ragweed pollen was shown to provoke asthma much more frequently than any of the other pollens (91). Children appear to be less sensitised to Ragweed pollen than adults are; only 5.9% of 507 asthmatic children aged between 1 and 17 years from a central Italian area had IgE antibodies to Ragweed species (92).
Ragweed pollinosis also has been documented in France (93-95). An epide-miological study of Ragweed allergy was conducted on 646 employees of 6 factories located in the Rhône valley south of the city of Lyon. In this study, 5.4% of subjects were symptomatic to Ragweed pollen, whereas 5.9% were shown to have allergen-specific IgE to this pollen (96). The spread of Ragweed in the middle Rhône area over the last ten years has been considerable; this is especially true of the Drome, along the river Rhône, but also of remote, very sheltered localities to the east and southeast of the province. Although Ragweed is said to grow only in the plains, in this area it appears to be extending into the mountains (97).
Ragweed has been found in the central region of Coahuila, Spain (98). In Canton Ticino, in the southern part of Switzerland, 17% of 503 consecutive patients suffering from hay fever were shown to be sensitised to Ragweed (99).
Ragweed pollinosis is very prevalent in Hungary. In the south of Hungary, among patients with hay fever symptoms during the late summer, 63% were sensitised to Ragweed pollen (100). In Budapest, 64.8% of allergic patients were sensitised to weed pollens, and 59% to Ragweed pollen (101). In other areas, Ragweed sensitisation has been shown to affect up to 83% of patients with late-summer seasonal allergic rhinitis (65).
Ragweed pollinosis is also spreading across Asia.
As Ragweed becomes widespread over China, Ragweed pollinosis tends to be more frequent. A survey of the distribution of Ragweed in the Qingdao district recorded that Ambrosia artemisiifolia was found to be widespread in many areas. Ragweed pollen was the chief allergen of the district and contributed over 18% of the total air-borne pollen in a year. IgE antibody determination with Ambrosia allergen extracts showed a prevalence of 67.7% in 624 pollen-allergic individuals (102).
Ragweed pollinosis is also prominent in Taiwan (103). Of 3,550 asthmatic patients who visited the Taipei Municipal Chung-shing Hospital, 52.3% were shown to be sensitised to Ragweed (104). A high prevalence of sensitisation to Ragweed pollen has been reported in a further study (105).
Ragweed pollinosis has also been documented in Korea (58,106) and Japan (107-108). In 226 children visiting a paediatric allergy clinic in Kyoto, Japan, 17.1% were shown to be sensitised to Ambrosia artemisiifolia (109).
Few studies have examined the prevalence of Ragweed sensitisation in South America. In Cartagena, Columbia, in 99 subjects with acute asthma and 100 controls, the prevalence of specific IgE to Short ragweed was shown to be 23% and 12% respectively (110).
Ragweed allergy has also been reported in northern New South Wales, Australia, where 70 of 153 atopic patients were sensitised to Ragweed, as shown by allergen-specific IgE determination (111).
Although Ragweed is not present in most of Africa, it has been shown to be the third most prominent allergen for asthmatics in Egypt (112).
The food supplement bee pollen has been previously found to cause anaphylactic reactions. It has been advertised as useful for ”everything from bronchitis to haemorrhoids.” This study describes an atopic patient who experienced a non-life-threatening anaphylactic reaction upon her initial ingestion of bee pollen. The preparation of bee pollen caused 52% inhibition of IgE binding to Short ragweed (113).
Compiled by Dr Harris Steinman, email@example.com.
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