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Delayed-onset erythematous skin reactions elicited in adult guinea pigs sensitized with protein antigens in incomplete Freund's adjuvant have been called "Jones-Mote" reactions to differentiate them from classic tuberculin type delayed hypersensitivity (1). However, this distinction has depended on relatively minor gross and microscopic differences and on the fact that JonesMote reactions, in contrast to delayed hypersensitivity, may be elicited only at early intervals after sensitization (2, 3). It is not surprising, therefore, that many workers have regarded Jones-Mote reactivity as a weak expression of delayed hypersensitivity (4).We have previously presented immunochemical and biologic data which permit a further distinction between Jones-Mote and classic delayed hypersensitivity reactions (5, 6). The two categories of reaction were shown to have different carrier requirements for hapten-specific sensitization but similar requirements for the expression of skin test reactivity. It was suggested that both reactions involve sensitized lymphoid cells, and that Jones-Mote reactions do not represent a combination of antigen with preformed antibody.We here demonstrate that Jones-Mote reactions have a unique light and electron microscopic morphology which is characterized by the accumulation of large numbers of basophilic leukocytes in the dermis. We prefer to designate

Using a sensitive single isotope enzymatic assay we measured bronchoalveolar lavage (BAL) fluid histamine in asymptomatic normal (nonallergic), allergic rhinitic, and allergic asthmatic subjects. Normal subjects were found to have little or no detectable amounts of histamine in BAL fluid (11±11 pg/ml), and few BAL fluid mast cells. In comparison, the allergic rhinitics and allergic asthmatics had much higher amounts of BAL fluid histamine (113±53 and 188±42 pg/ml, respectively), and a significantly greater number of BAL fluid mast cells. Furthermore, despite having equivalent baseline pulmonary function values, allergic asthmatics with BAL fluid histamine levels > 100 pg/ ml required only 7±2 breath units of methacholine to induce a 20% drop in forced expiratory volume in 1 s (FEV1) (PD" FEV1) while asthmatics with BAL fluid histamine levels < 100 pg/ml required 49±19 breath units (P < 0.05). These data suggest that allergic asthmatics have ongoing lung mast cell degranulation that might contribute to the etiology of airway hyperresponsiveness.