Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy characterised by extensive stromal remodelling. Recent efforts in normalisation of specific fibroblasts and immune populations have demonstrated therapeutic benefits in pre-clinical models, whereas genetic depletion of fibroblasts resulted in accelerated disease progression. Such disparate responses highlight an urgent need for a better understanding of context-specific roles of tumour-stroma crosstalk in PDAC function and therapeutic response. Here, using co-cultures of murine pancreatic cancer cells (PCCs), fibroblasts/stellate cells (PSCs) and macrophages (MΦs), we demonstrate that PCC-PSC-MΦ crosstalk creates an inflammatory niche, in which excessive levels of tumour-promoting soluble factors such as members of IL6 family, CXC- and CC-chemokines are secreted. Further, we identify that the PSC compartment is the cellular source of such inflammatory factors from PCC-PSC-MΦ co-culture, in which PSCs undergo reprogramming of inflammatory (iCAF) polarity with expression of immunomodulatory receptors and ligands, an observation recapitulated in single cell RNAseq analysis of murine PDAC tumours. Mechanistically, we show that heterocellular OSM-OSMR signalling is a key regulator of iCAF polarity. Macrophage-secreted Oncostatin M (OSM) engages with its cognate receptor, OSMR, expressed in fibroblasts and potently induces iCAF polarity via activating JAK-STAT pathway and antagonising myofibroblast-like phenotype. OSM can synergistically shift fibroblasts into iCAF polarity with other macrophage-secreted factors such as TNFa and IL1B. We also show that tumour cell-derived GM-CSF regulates OSM secretion in macrophages. Importantly, phosphoproteomic analysis shows that iCAF polarity reciprocally regulates distinct signalling pathways in tumour cells with enhanced signalling through the JAK/STAT, Erk1/2, Akt, p38 and PKA pathways. Furthermore, our preliminary data show that the OSM-mediated iCAF polarity dictates metastatic potential in a syngeneic orthotopic mouse model. These findings identify heterocellular GM-CSF-OSM-OSMR axis as a mediator of inflammatory fibroblast polarity, which may be targeted to modulate the reciprocal signals and metastatic potential elicited in the tumour cells.