PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14729754-0	2004	Dicloxacillin and erythromycin at high concentrations increase ICAM-1 expression by endothelial cells: a possible factor in the pathogenesis of infusion phlebitis.	Erythromycin	18-30	intercellular adhesion molecule 1	Homo sapiens	63-69	
21038022-13	2010	Erythromycin given in group II decreased the levels of IL-8 and ICAM-1.	Erythromycin	0-12	intercellular adhesion molecule 1	Homo sapiens	64-70	
19052724-16	2009	A concentration of 800 mg/L erythromycin medium caused an increase of the expression of CD34 (+6%), E-selectin (+5%), ICAM-1 (+14%) and VCAM-1 (+5%).	Erythromycin	28-40	intercellular adhesion molecule 1	Homo sapiens	118-124	
14729754-7	2004	RESULTS: Despite constitutive expression of ICAM-1 (34%) in HUVEC, 6250 mg/L of dicloxacillin or erythromycin significantly increased the number of cells with ICAM-1 expression by 37% and 30%, respectively.	Erythromycin	97-109	intercellular adhesion molecule 1	Homo sapiens	44-50	
14729754-7	2004	RESULTS: Despite constitutive expression of ICAM-1 (34%) in HUVEC, 6250 mg/L of dicloxacillin or erythromycin significantly increased the number of cells with ICAM-1 expression by 37% and 30%, respectively.	Erythromycin	97-109	intercellular adhesion molecule 1	Homo sapiens	159-165	
12828863-7	2003	On the other hand, RV infection is inhibited by treatment with soluble ICAM-1, and by reduction of ICAM-1 expression in the airway epithelial cells after treatment with erythromycin.	Erythromycin	169-181	intercellular adhesion molecule 1	Homo sapiens	99-105	
11956054-4	2002	Erythromycin reduced the supernatant RV14 titers, RV14 RNA, the susceptibility to RV14 infection, and the production of ICAM-1 and cytokines.	Erythromycin	0-12	intercellular adhesion molecule 1	Homo sapiens	120-126	
11956054-7	2002	These results suggest that erythromycin inhibits infection by the major RV subgroup by reducing ICAM-1 and infection by both RV subgroups by blocking the RV RNA entry into the endosomes.	Erythromycin	27-39	intercellular adhesion molecule 1	Homo sapiens	96-102	
11956054-8	2002	Erythromycin may also modulate airway inflammation by reducing the production of proinflammatory cytokines and ICAM-1 induced by RV infection.	Erythromycin	0-12	intercellular adhesion molecule 1	Homo sapiens	111-117	
10051731-9	1999	Histopathological studies revealed that erythromycin markedly decreased neutrophils in the lung and skin lesions and myeloperoxidase in the lung, simultaneously with inhibiting ICAM-1 expression.	Erythromycin	40-52	intercellular adhesion molecule 1	Homo sapiens	177-183	
10051731-12	1999	CONCLUSIONS: The therapeutic dosage of erythromycin significantly suppressed acute neutrophil influx into the lung, intradermal Arthus reaction and the expression of ICAM-1 in the lesions of experimental EAA.	Erythromycin	39-51	intercellular adhesion molecule 1	Homo sapiens	166-172